脂连素抑制人前列腺癌细胞氧化应急 Adiponectin inhibits oxidative stress in prostate carcinoma cells
ORIGINAL ARTICLE
Adiponectin inhibits oxidative stress in human prostate carcinoma cells
J-P Lu 1,2,ZF Hou 1,2,WC Duivenvoorden 1,2,K Whelan 1,2,A Honig 1,2and JH Pinthus 1,2
1
Division of Urology,Department of Surgery,McMaster University,Hamilton,Ontario,Canada and 2Department of Surgical Oncology,Juravinski Cancer Centre,Hamilton,Ontario,Canada
BACKGROUND:Emerging data suggest that obesity increases the risk of aggressive prostate cancer (PC),but the mechanisms underlying this relationship remain to be fully elucidated.Oxidative stress (OS)is a key process in the development and progression of PC.Adiponectin,an adipocyte-specific hormone,circulates at relatively high levels in healthy humans,but at reduced levels in obese subjects.Moreover,case–control studies also document lower levels of serum adiponectin in PC patients compared with healthy individuals.
METHODS:Human 22Rv1and DU-145PC cell lines were examined for the generation of OS and detoxification of reactive oxygen species after treatment with adiponectin.Normality was confirmed using the Shapiro–Wilk test and results were analyzed using a one-way analysis of variance.
RESULTS:We demonstrate that adiponectin increased cellular anti-oxidative defense mechanisms and inhibited OS in a significant and dose-dependent manner.We show that adiponectin treatment decreased the generation of superoxide anion in both cell lines,whereas the transcript levels of NADPH oxidase (NOX)2and NOX4increased.We also found indications of an overall anti-oxidative effect,as the total anti-oxidative potential,catalase activity and protein levels,and manganese superoxide dismutase protein levels increased significantly (P o 0.05)in both cell lines after treatment with adiponectin.CONCLUSION:Lower levels of adiponectin in obese individuals may result in higher levels of prostatic OS,which may explain the clinical association between obesity,hypoadiponectinemia and PC.
Prostate Cancer and Prostatic Diseases advance online publication,17January 2012;doi:10.1038/pcan.2011.53
Keywords:adiponectin;obesity;oxidative stress
Introduction
Cancer initiation and progression are influenced by intrinsic tumor-dependent factors.However,host factors can influence the individual environment in which each specific tumor grows and its potential to progress.Obesity,a classic host factor,is known to increase the risk of prostate cancer (PC).Findings from large prospective cohort trials indicate that men with higher body mass index are more likely to be diagnosed with aggressive PC and are at higher risk of PC-related death compared with men having normal body mass index.1–4Reasons for these findings are likely multi-factorial and include detection bias (lower PSA levels and larger prostates 5and difficult digital rectal examination in overweight patients),which leads to delayed diagno-sis.Other reasons may relate to an unfavorable
pro-proliferative hormonal profile with higher insulin and insulin growth factor levels 5and a poor diet with excess calories,5dietary fat 6and refined carbohydrate intake.7
The adipose tissue is the largest endocrine organ in mammals,producing a vast number of hormones,collectively referred to as adipokines.The blood levels of one of these hormones,adiponectin,are inversely related to body weight,and are reduced in obese patients.8,9Several case–control studies have documen-ted that lower levels of adiponectin are associated with increased incidence and aggressiveness of PC.10–14However,the mechanisms responsible for the tumor-suppressive effects of adiponectin are not clear.
Oxidative stress (OS)triggers a host of pro-carcino-genic processes and is a key event in the initiation,development and progression of PC.It is caused by an imbalance between the production of reactive oxygen species (ROS)and their detoxification by enzymes,such as catalase and manganese superoxide dismutase (MnSOD).OS related to age,15inflammation and nutri-tion,16as well as exposure to androgens,17leads to pro-carcinogenic events,in particular accumulation of oxidative DNA damage.Likewise,it has been suggested
Received 23June 2011;revised 6September 2011;accepted 25September 2011Correspondence:Dr JH Pinthus,Department of Surgical Oncology,Juravinski Cancer Centre,699Concession Street,Hamilton,Ontario,Canada L8V 5C2.
E-mail:jehonathan.pinthus@jcc.hhsc.ca
Prostate Cancer and Prostatic Diseases (2012),1–8
&2012Macmillan Publishers Limited All rights reserved 1365-7852/https://www.wendangku.net/doc/354692651.html,/pcan
that compared with normal subjects or patients with BPH,PC patients have a systemic imbalance in their OS/anti-oxidant status.18
There are two major sources of cellular ROS.The main source is the mitochondria,which is coupled to fatty acid oxidation and the family of NADPH oxidase(NOX) enzymes that transport electrons across biological mem-branes to generate superoxide O2áàby the reduction of oxygen.19Another cellular source of ROS,albeit to a lesser extent,are the peroxisomes.Owing to the presence and action of xanthine oxidase,peroxisomal ROS consist predominantly of superoxide anion radicals.20Adipo-nectin has been shown to activate50AMP-activated protein kinase(AMPK).21–23Activated AMPK phosphor-ylates and inactivates the main regulator of mitochon-drial fatty acid oxidation acetyl-CoA carboxylase(ACC). As ACC in turn converts acetyl-CoA to malonyl-CoA,an inhibitor of carnitine palmitoyltransferase1,the rate-limiting enzyme for mitochondrial fatty acid oxidation, adiponectin is expected to stimulate mitochondrial fatty acid oxidation and hence mitochondrial production of ROS.The main cellular detoxification mechanism of ROS is enzymatic.SOD is considered to be the primary defense mechanism,as it converts superoxide,a highly reactive ROS and a strong initiator of oxidative chain reaction,to hydrogen peroxide.Hydrogen peroxide must then be reduced to water by catalase in order to prevent the formation of hydroxyl radicals.
To delineate the mechanisms responsible for the tumor-suppressive effects of adiponectin in PC,we investigated whether adiponectin,a hormone that has been shown to circulate at lower levels in obese and PC patients,has a protective role against the generation of OS in PC cells.We thus focused on the effects of adiponectin on production of the superoxide anion and expression of NOX,the major source of ROS in PC cells24 on the one hand,and on the expression and activity of SOD and catalase on the other.
Materials and methods
Cell lines
Human prostate adenocarcinoma DU-145and22Rv1cell lines were obtained from ATCC(Manassas,VA,USA). The DU-145cell line was originally derived from a brain metastasis from a prostate adenocarcinoma patient.25 The cells are androgen-independent,do not express PSA and represent an aggressive PC cell line,whereas22Rv1 cells were derived from a PC xenograft that relapsed during androgen withdrawal.22Rv1cells are considered less aggressive,are androgen-responsive and express PSA.26Cells were propagated in RPMI1640medium supplemented with10m M4-(2-hydroxyethyl)-1-piperazi-neethanesulfonic acid,1.0m M sodium pyruvate(Sigma-Aldrich,Oakville,Ontario,Canada)and10%fetal bovine serum(Invitrogen,Burlington,Ontario,Canada).Cells were cultured at371C in a humidified atmosphere con-taining5%CO2.
Adiponectin treatment
Full-length human recombinant adiponectin(BioVendor, Candler,NC,USA)was used to treat human PC cell lines.Optimization experiments were conducted to determine the effective concentrations of adiponectin for each cell line.To avoid interference of adiponectin present in fetal bovine serum,all experiments were conducted in serum-free RPMI1640or Opti-MEM medium(Invitrogen)following a minimum of24h of culture in serum-free medium.
Superoxide anion production
PC cells were seeded at40000cells per well in a96-well plate.After culture for24h in serum-free medium, adiponectin was added at20or40m g ml–1in Opti-MEM medium.After another24h,intracellular superoxide anion production was detected by the nitroblue tetrazolium(NBT)assay(Sigma-Aldrich).Upon reduction,the yellow water-soluble NBT changed to dark-blue insoluble formazan.Cells were incubated for 90min at371C and5%CO2in phosphate-buffered saline(PBS)containing0.2%NBT.Wells were washed twice with PBS and formazan was dissolved in60m l2M KOH and70m l DMSO by sonication for10min. Absorbance was measured using a microplate reader at 620nm.27,28The results were normalized to cell number using the WST-1assay(Roche Diagnostics,Laval, Quebec,Canada)and were expressed as percentage of untreated control.
Quantitative reverse transcriptase-PCR
Human22Rv1and DU-145PC cells were treated with 20m g ml–1adiponectin for24h.Total RNA was isolated using the RNeasy mini-kit(Qiagen,Mississauga,Ontario, Canada).To determine the relative expression,RNA was reverse-transcribed using200ng of total RNA in the presence of Superscript II RT(200U,Invitrogen)using oligo(dT)12àhttps://www.wendangku.net/doc/354692651.html,plementary DNA was amplified in a total volume of50m l using the iQ Sybr Green kit(BioRad Laboratories,Mississauga,Ontario,Canada)in Tris-HCl (20m M)and50mmol KCl(pH8.3),dNTPs(0.2m M), 1.2U Taq DNA polymerase(BioRad Laboratories)and gene-specific primers(500nmol)for NOX2and NOX4. The sequences for the NOX2and NOX4primer pairs were obtained from Vaquero et al.29The reactions were carried out in a Mini-Opticon thermal cycler(BioRad Laboratories).PCR was started by a3-min denaturation at951C,followed by35cycles of25-s annealing at621C, 25-s extension at721C and30-s denaturation at941C. In each PCR run,500nmol of primers for b-actin were used as internal control as previously described.30 The2àDD C t method was used to calculate relative expression levels.
Anti-oxidant assays
Human PC cells were seeded at5?105cells per well in a six-well plate.After adiponectin treatment,the cells were washed twice with PBS.The cells were collected in 1ml ice-cold PBS by scraping,lysed by sonication, followed by centrifugation at10000g for15min. The protein concentration in the supernatant was determined using the DC protein concentration determi-nation kit(BioRad Laboratories).Total anti-oxidant potential in lysates(20m g)was measured using a colorimetric quantitative assay kit(OxisResearch,
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Beverly Hills,CA,USA),which is based on the reduction of Cu2tto Cutcontributed by all anti-oxidants present. The chromogenic reagent selectively forms a2:1complex with Cut,which has a maximum absorbance at450nm. Uric acid was used to obtain a calibration curve.The anti-oxidant potential was calculated as m M uric acid equivalents per ml.
Catalase activity in the cell lysates(10m g)was determined using a commercially available kit,following the manufacturer’s instructions(Cayman Chemicals, Ann Arbor,MI,USA).The catalase assay is based on the reaction with methanol in the presence of H2O2.The formaldehyde produced was measured spectrophotome-trically using the chromogen purpald,which upon oxidation changes from colorless to a purple color.The catalase activity was determined using a standard curve of formaldehyde.
Western blot analysis
PC cells seeded at5?105cells per well in the six-well plate were treated with adiponectin for24h.The cells were washed with PBS,collected and centrifuged at450g for5min at41C.The pellet was resuspended in NP40 lysis buffer(50mmol l–1Tris(pH7.6),150mmol l–1NaCl, 1%NP40,10%glycerol,proteinase inhibitor cocktail (Sigma-Aldrich))for30min at41C.The lysates were centrifuged at10000g for10min at41C,the supernatant was collected and the protein concentration determined. Cell lysate(20m g)was resolved by12%SDS-polyacryla-mide gel electrophoresis and proteins were transferred onto a polyvinylidene fluoride membrane(Millipore, Billerica,MA,USA).After blocking non-specific binding sites with TBST containing5%skim milk,the membrane was incubated with the primary antibody(1:1000,rabbit anti-AdipoR1,anti-AdipoR2(Abbiotech,San Diego,CA, USA)),rabbit anti-phospho(Ser79)-acetyl-CoA-carboxy-lase,rabbit anti-AMPK or anti-phospho(Thr172)-AMPK (Cell Signaling Technology,Danvers,MA,USA),rabbit anti-catalase(Millipore)and rabbit anti-MnSOD(Abcam, Cambridge,MA,USA).The secondary antibody con-jugated with horseradish peroxidase(1:3000;Jackson ImmunoResearch Laboratories,West Grove,PA,USA) was used in conjunction with chemiluminescence detec-tion(Pierce SuperSignal Pico Chemiluminescent,Fisher Scientific,Ottawa,Ontario,Canada).An antibody specific for b-actin(1:1000,Sigma-Aldrich)served as internal control.The relative amount of MnSOD or catalase protein expression was normalized to the amount of actin using densitometry.
Statistical analysis
Statistical analysis was performed using STATA SE11.0 (College Station,TX,USA).Normality was confirmed by the Shapiro–Wilk test.The normally distributed data were analyzed using a one-way analysis of variance test. The data that were not normally distributed(superoxide anion production results,protein expression data,and the catalase activity data for the22Rv1cell line)were analyzed by the Mann–Whitney U-test.The DD C t values were analyzed using a non-parametric Wilcoxon-signed rank test.A P-value o0.05was regarded as significant. P-values o1?10à4are given as P o0.0001.Results
We measured the generation of OS and the expression
and activity of several enzymes involved in the detox-ification of ROS in two human prostate adenocarcinoma
cell lines,22Rv1and DU-145.We first determined the production of superoxide anion after adiponectin treat-
ment by the reduction of NBT.Treatment of human
22Rv1PC cells with full-length adiponectin decreased
the generation of superoxide in a dose-dependent manner by43%and46%at20and40m g ml–1adiponec-
tin,respectively(Figure1a).Similarly,in DU-145cells, adiponectin also decreased the generation of superoxide
anion by22%and32%at20and40m g ml–1adiponectin, respectively(Figure1b).The inhibition reached statistical significance at the concentration of40m g ml–1for both
22Rv1and DU-145cells as shown in Figure1(P?0.02
and0.01,respectively).As an indirect measure of superoxide anion generation,we also determined the transcript levels of the NOX enzymes,NOX2and NOX4,
after treatment with full-length adiponectin for24h by quantitative reverse transcriptase-PCR.The generation of mitochondrial ROS is coupled to fatty acid oxidation.
The family of NOX enzymes transfers electrons from NADPH across biological membranes to generate super-
oxide anion.Interestingly,treatment with adiponectin induced a significant increase in the transcript levels
of
Figure1Inhibitory effect of adiponectin on oxidative stress. Human prostate cancer cells were treated with0,20or40m g ml–1 adiponectin for24h in serum-free medium and the production
of superoxide anion was measured using the nitroblue tetra-
zolium reduction assay.(a)22Rv1cells.(b)DU-145cells.Data represent mean±s.d.from two independent experiments carried
out in triplicate.Statistically significant differences as determined
using a two-tailed Mann–Whitney U-test are indicated by the
P-values.
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NOX2and NOX4in both human PC cells by 10–80-fold (Figure 2).Figure 3a shows that both PC cell lines express AdipoR1and AdipoR2,the receptors through which adiponectin’s signal is transduced.31,32A well-character-ized molecular pathway in adiponectin signaling in PC cells is through the activation (phosphorylation)of AMPK.23Using human 22Rv1PC cells,we confirmed that full-length adiponectin was able to phosphorylate and activate AMPK,without affecting the amount of AMPK.At 20m g ml –1adiponectin,P-AMPK,normalized for the expression of b -actin,increased 2.2-fold compared with the levels found in untreated control cells.The activation of AMPK consequently led to an almost fourfold increase in the phosphorylation of its downstream target ACC (Figure 3b),which is inhibitory to its activity .
Concomitantly,we determined the total cellular anti-oxidative potential after adiponectin treatment by mea-suring the reducing potential of all anti-oxidants present in the sonicated lysate samples from both PC cell lines.Adiponectin significantly increased the anti-oxidative potential in a dose-dependent manner in both 22Rv1and DU-145cells (P o 0.0001)(Figure 4).Similarly,we examined whether adiponectin treatment affected the protein expression and activity of catalase,one of the key anti-oxidative enzymes involved in the detoxification of hydrogen peroxide.Indeed,treatment with adiponectin significantly and dose-dependently increased the expres-sion of catalase,by approximately twofold at 40m g ml –1adiponectin,in both cell lines (Figures 5a–c).This translated into a significantly increased activity of the enzyme,as measured spectrophotometrically against formaldehyde as a standard (Figures 5d and e).Furthermore,the protein expression of MnSOD,an important enzyme in the mitochondrial matrix that dismutates superoxide anion to generate hydrogen peroxide,was also found to be significantly elevated in both PC cell lines after treatment with adiponectin (P o 0.05)(Figure
6).
Figure 2Effect of adiponectin on NADPH oxidase (NOX)mRNA expression.Relative gene expression of NOX2and NOX4in DU-145and 22Rv1PC cells treated with 0or 20m g ml –1adiponectin for 24h in serum-free medium,as determined by quantitative RT-PCR.Total RNA was isolated,cDNA was reverse-transcribed using oligo-dT primers and RT-PCR was performed using NOX -specific primers.The difference in threshold cycle (D C t )between the gene of interest and the internal control (b -actin)was used to calculate the relative fold expression (2àDD C t ±s.d.)compared with the expression in corresponding untreated control cells.All experiments were carried out at least three times independently in duplicate.*Statistically significant differences were determined using the Wilcoxon signed-rank test (P o
0.05).
Figure 3Expression of adiponectin receptors and effects of adiponectin on 50AMP-activated protein kinase (AMPK)signaling in human PC cells.(a )Protein expression of AdipoR1and AdipoR2in cell lysates (20m g)of human 22Rv1and DU-145prostate cancer (PC)cells as determined by western blot analysis.(b )Treatment with 1and 20m g ml –1adiponectin for 1h increases phosphorylation of AMPK and acetyl-CoA carboxylase (ACC)in 22Rv1PC cells,as determined by western blot analysis.Antibodies specific for AdipoR1,AdipoR2,AMPK a ,P(Thr172)-AMPK a ,P(Ser79)-ACC and b -actin were
used.
Figure 4Adiponectin increases the anti-oxidant potential.Human prostate cancer cells were treated with 0,20or 40m g ml –1adiponectin for 24h in serum-free medium and the total anti-oxidant potential was measured in (a )22Rv1and (b )DU-145cell lysates.Data represent mean ±s.d.from at least two independent experiments carried out in triplicate.Statistically significant differences as determined using a one-way analysis of variance are indicated by the P -values.
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Discussion
We investigated the effects of adiponectin on OS in human PC cells.OS caused by an imbalance between the production of ROS and their detoxification leads to pro-carcinogenic events.On the one hand,we measured both the production of superoxide anion and the expression of the main two enzymes responsible for the production of superoxide anion after adiponectin treatment.Treatment of 22Rv1and DU-145PC cells with adiponectin decreased the generation of superoxide in a dose-dependent manner (Figure 1).The transcript levels of NOX2and NOX4after treatment with adiponectin were signficantly induced in both DU-145and 22Rv1PC cells
(Figure 2),suggesting that the generation of superoxide anion in 22Rv1and DU-145is mainly through a pathway other than NOX2and NOX4.Protein expression of NOX2and NOX4was not undertaken because of a lack of suitable antibodies.
On the other hand,we also determined the total cellular anti-oxidative potential after adiponectin treat-ment by measuring the reducing potential of all anti-oxidants present in the lysate samples from both PC cell lines.Adiponectin increased the anti-oxidative potential in a dose-dependent manner (Figure 4),explaining in part the larger decrease in superoxide anion levels (Figure 1)despite elevated transcript levels of NOX2and NOX4(Figure 2).Moreover,adiponectin
also
Figure 5Adiponectin increases the protein expression and activity of catalase.Human 22Rv1PC cells were treated with 0,20or 40m g ml –1adiponectin for 24h in serum-free medium.(a )Catalase protein expression was determined by western blot analysis using an antibody specific for catalase.Protein expression data from at least two experiments were quantified and normalized for the expression of b -actin by densitometric analysis.The mean relative expression ±s.d.is shown in (b )for 22Rv1cells,and in (c )for DU-145cells.Catalase activity was measured in (d )22Rv1and (e )DU-145cell lysates.Data represent mean ±s.d.from three independent experiments carried out in triplicate.Statistically significant differences as determined using a one-way analysis of variance or two-tailed Mann–Whitney U -test (in the case of the 22Rv1cells)are indicated by the P -values.
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induced a significant elevation in the protein expression of MnSOD (Figure 6)and the activity and protein expression of catalase in both cell lines (Figure 5).
Overall,the results of this in vitro study indicate that adiponectin exerts anti-oxidative effects in PC cells.We demonstrate that these effects of adiponectin are dose-dependent and are mediated by the induction of anti-oxidative enzymatic defense mechanisms.It is reasonable to believe that adiponectin actually stimulates the production of ROS.Mitochondrial ROS is coupled to fatty acid oxidation and the family of NOX enzymes that transport electrons across biological membranes to generate superoxide anion by the reduction of oxygen.33Adiponectin treatment is expected to stimulate mito-chondrial fatty acid oxidation and hence mitochondrial production of ROS through its phosphorylation and activation of AMPK.21–23Activated AMPK inactivates ACC through phosphorylation on serine 79.ACC converts acetyl-CoA to malonyl-CoA,which in turn inhibits the rate-limiting enzyme for mitochondrial fatty acid oxidation,carnitine palmitoyltransferase 1.As shown,adiponectin also increases the mRNA expression of NOX2and NOX4enzymes (Figure 2).Thus,although adiponectin may increase the generation of ROS,through both inhibition of ACC (Figure 3)and increase in NOX expression (Figure 2),the end effect is that the levels of OS in PC cells are suppressed (Figure 1)through the augmentation of their anti-oxidative capacity (Figures 4,5,and 6).
OS elicits pro-carcinogenic events in initiation,devel-opment and progression of PC.One limitation of our study is the use of human PC cell lines,which would
suggest that adiponectin has a role in PC progression rather than in cancer initiation.To investigate the events during initiation,normal prostate epithelial cells would appear to be a better choice.However,the available models have significant limitations.PNT1A,human adult prostate epithelial cells immortalized with SV40large-T antigen,demonstrate c-myc gene amplifications and therefore do not truly represent normal cells.Primary prostate epithelial cells have very limited and unpredictable growth capacity in culture and are not suitable for carrying out the experiments.
OS is a facilitating event in the development of PC.Accordingly,cells under OS may manifest continuous genetic alterations that can lead to carcinogenesis.34In particular,the aging prostate,which is exposed to androgenic,inflammatory and nutritional OS-generating insults,35often suffers from inherent insufficient capacity to neutralize OS in men prone to develop PC.For example,inactivation of the pi-class glutathione S-transferase gene GSTP1by promoter hypermethylation appears to uniformly accompany human prostatic carcinogenesis.36Thus,by increasing the expression and activity of catalase and MnSOD,adiponectin may supplement the cellular anti-oxidative capacity to over-come the accumulation of ROS mediated by its own effects (mitochondrial respiration and NOX activity)as well as by processes such as aging,inflammation and nutritional factors that link OS generation and develop-ment of PC.Our study,which shows that adiponectin increased the cellular anti-oxidant potential in vitro,may also have implications for the treatment of PC.As part of their primary mode of action,radiation and
many
Figure 6Adiponectin increases the protein expression of manganese superoxide dismutase (MnSOD).Human prostate cancer cells were treated with 0,20or 40m g ml –1adiponectin for 24h in serum-free medium and MnSOD expression was determined by western blot analysis using an antibody specific for MnSOD (a ).MnSOD protein expression data from three experiments were quantified and normalized for the expression of b -actin by densitometric analysis.The mean relative expression ±s.d.is shown in (b )for 22Rv1,and in (c )for DU-145cells.Statistically significant differences as determined using a two-tailed Mann–Whitney U -test are indicated by the P -values.
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chemotherapy agents induce OS,directly or indirectly, resulting in apoptosis.One could thus hypothesize that patients with lower serum adiponectin levels have higher susceptibilities to such treatments when com-pared with patients with higher serum adiponectin levels,a hypothesis that needs to be examined in prospective randomized clinical trials.
The mechanism implied by the results of our study may explain the link between hypo-adiponectinemia and PC that was demonstrated in case–control studies.10,11,14 Maximizing adiponectin signaling appears logical as a translational possibility in PC.Unfortunately,treatment with adiponectin per se is impractical,as it has a short half-life,is present at high circulating levels,and large-scale production of the native forms of full-length adiponectin with all post-translational modifications is a difficult task.37However,several other strategies to maximize adiponectin signaling are currently under investigation.Moreover,whether obese patients who generally have lower circulating levels of adiponectin also suffer from higher levels of prostatic OS remains to be determined.Nevertheless,the results of this study propose a potential link between obesity and prostatic OS,portraying a possible mechanistic link between obesity and PC.
Conflict of interest
The authors declare no conflict of interest.
Acknowledgements
This study was funded by grants to JHP by the Juravinski Cancer Center Foundation and the Prostate Cancer Foundation of Canada.
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前列腺癌诊疗规范标准
.专业整理. .学习帮手. 前列腺癌诊疗规 前列腺癌一．临床诊断【一】症状前列腺癌在早期阶段可完全没有症状，当肿瘤发展使前列腺增大到一定体积，以及膀胱颈部发生梗阻时才出现症状。 此时的梗阻症状与前列腺增生无明显差别，表现为尿频、尿急、尿流缓慢、排尿困难、排尿不尽，甚至发生尿潴留等症状。 但在症状的变化过程中，值得注意的是前列腺癌病情进展较快，而前列腺增生很缓慢。 前列腺癌血尿不常见，一般仅见于前列腺导管癌或移行细胞癌。 在临床工作中，前列腺癌病人往往是因其他部位转移灶引起的不适而就诊，在体格检查或特殊检查时确诊的。 其症状因转移的部位不同而不同。 当肿瘤压迫或发生周围淋巴结转移造成淋巴管阻塞或压迫血管时；或因癌相关性血液高凝状态而发生下肢深静脉血栓时，可出现下肢水肿。 骨转移可为多发性的，一般以腰骶部和骨盆多见，表现为持续性骨痛、下肢活动障碍、易疲劳，严重者可出现下肢瘫痪。 当肿瘤侵犯或压迫周围神经或脊髓时，可出现局部神经疼痛如会阴部疼痛或神经功能障碍。 有肺转移时可有气短等肺部症状。 直肠受累时可有大便困难、肛门坠胀感。 其他还有贫血等。
【二】体格检查 1．直肠指检前列腺直肠指检是诊断前列腺癌的主要方法之一，若结合前列腺穿刺活检，60％左右的病人可获得诊断。 因病灶多发生于前列腺的后叶及两侧叶的移行区，质地坚硬，直肠指检时常能触及硬结。 检查时应注意前列腺的大小、质地、有无硬结或呈结节样改变、中间沟以及精囊情况。 早期前列腺癌虽无临床症状，但直肠指诊可以发现较小病灶。 据报道直肠指检时前列腺部触及硬结，在 50 岁以上者 50％为癌；如硬结延及精囊，前列腺边缘分界不清者 70％为癌。 也有报道前列腺癌直肠指检可漏诊 40％以上的局限性癌灶。 前列腺癌直肠指检对于前列腺癌的分期有一定帮助，直肠指检可初步检出前列腺外的浸润情况，但常常估计过低。 2．其他对于所有的癌症病人均应进行全面、仔细的体格检查，包括浅表淋巴结的触诊。 当病人诉有骨痛时应对触痛点进行仔细的骨骼检查。 检查时还需与前列腺结石、非特异性肉芽肿性前列腺炎、局灶性前列腺结核以及良性前列腺增生症相鉴别。 【三】实验室检查 1．细胞黏附抑制试验前列腺癌病人白细胞黏附抑制试验的阳性率可达 77％一 89％。 最常用的方法有白细胞计数板法、试管法和
老年患者腹腔镜前列腺癌根治术后的护理
老年患者腹腔镜前列腺癌根治术后的护理 顾峥峥，孟晓敏 ［摘要］目的总结分析老年患者腹腔镜前列腺癌根治术的护理经验。方法对16例行腹腔镜前列腺癌根治术的老年患者实施术前、术后系统化整体护理。结果本组患者手术均成功，无重大护理并发症发生。结论整体护理可以使老年患者在腹腔镜前列腺癌根治术后恢复中获益。 ［关键词］前列腺肿瘤；腹腔镜手术；整体护理；老年 ［中图分类号］R697.3［文献标识码］B doi:10.3969/j.issn.1674-3245.2012.02.024 前列腺癌是威胁男性健康的常见肿瘤之一，2002年全球新发病例679000例，位列男性肿瘤的第2位，且其发病率仍呈上升趋势［1］。腹腔镜下前列腺癌根治术是最新的一种治疗前列腺癌的微创技术，是通过腹腔镜的辅助,直视腹腔，利用超声刀、高频电刀等达到前列腺癌根治的目的。与传统手术方法相比，与开放手术相比,腹腔镜手术中远期肿瘤根治效果相当，但创伤相对更小、患者恢复更快［2］。特别对老年患者，腹腔镜提供了一种相对安全的手术方式。2008年～2011年我科应用腹腔镜手术对16例老年前列腺癌患者在责任制护理的基础上进行系统化整体护理，取得良好效果。 1对象与方法 1.1对象16例前列腺癌患者，年龄60~76岁，平均（68.5±5.0）岁。经直肠B超引导下前列腺穿刺活检证实为前列腺腺癌，术前均行心、肺、肝肾功能和凝血功能等常规检查，均于腹腔镜下行前列腺癌根治术。 1.2方法应用先进的系统化整理护理理念，与责任制护理相结合，针对老年患者的特点，专人实行24h的责任护理，并增加每班对患者情况及需要解决问题的评估。另外，根据系统化整体护理的要求，以患者为中心，制定了详尽、完善的护理计划，以期简化书写程序,省时节力，以便更好地护理患者。 2结果16例患者术后均无尿失禁和排尿困难，无下肢静脉血栓、肺部感染等护理并发症的发生，随访2~18个月，所有患者生存良好，未发现局部复发和远处转移。 3护理 3.1术前护理根据系统化整体护理要求，制定了具体的术前护理计划，并派1名责任护士全程实施。（1）术前宣教：针对老年患者的特点，术前宣教工作需要更为细心、全面。在术前即指派专人对患者进行疾病相关知识的简单讲解，对手术前的准备，手术后的注意事项进行宣教，指导患者有效咳痰的方法,讲解术后预防肺部感染、下肢静脉血栓及功能锻炼的方法，并要求患者加以练习。需要进监护室的患者，提前参观监护室，对术后环境的改变提前适应，对术后床旁的监护仪器提前了解，减轻患者的术前恐惧感及术后因环境陌生造成的不安全感。（2）心理护理：整体护理的要求是面向整体的人，即不仅把疾病与患者视为一个整体，还应把生物学的人与社会、心理学的人视为一个整体。腹腔镜前列腺癌根治术是一项近年开展的手术，患者对手术方式及过程不了解，表现为焦虑、恐惧。老年患者由于反应、思维迟缓，理解能力及适应能力的减低，因此要比年轻人术前更害怕手术产生的疼痛或担心手术后遗症，进而术前产生一系列的恐惧、害怕的心理，直接影响手术的效果以及疾病的恢复［3］。由专人向患者介绍腹腔镜手术的优点,耐心地解答患者疑问,鼓励患者以正确的态度对待手术。（3）术前准备：术前常规抗生素皮试并静脉输注,备皮。术前1d进半流食,并分别在15∶00、20∶00口服50%硫酸镁溶液30ml，饮水1000ml做肠道准备。术晨禁食、禁水,行清洁灌肠,术晨穿抗血栓弹力袜。 3.2术后护理术后护理是患者能否康复的关键。根据系统化整体护理方案，由专人实施护理全过程，包括出院指导及出院后的随访，以期患者早日康复。 3.2.1常规护理按全麻后护理常规进行,术后去枕平卧,头偏向一侧，6h后协助取半卧位，行心电、血压、脉搏及血氧饱和度监测，并准确记录24h出入量。 3.2.2术后疼痛护理给予患者心理安慰，必要时使用镇痛泵或镇痛药。 3.2.3耻骨后引流管护理耻骨后引流管对观察有无术后出血及吻合口瘘有重要意义，注意保持引流管通畅，妥善固定,定时挤压，避免打折、扭曲、堵塞，注意观察引流液颜色、性质和量的变化并做好记录。若其在短时间内引流出大量鲜红色液体并伴有腹痛、腹胀、腹膜刺激等症状，应警惕术后继发出血，若其有清淡引流物则可能提示尿道膀胱吻合口瘘，均应及时报告医师处理。 3.2.4导尿管护理术后导尿管保留时间较长，约3周，以利于尿道连续性的恢复，防止吻合口狭窄，保持尿道口清洁，以防逆行感染。 3.2.5潜在并发症的护理（1）高碳酸血症：高碳酸血症是腹腔镜手术较独特的并发症，形成气腹所需的CO2进入血液循环，若手术时间过长，患者可出现一过性高碳酸血症。术 基金项目：解放军总医院护理部科研立项课题（2010YH07） 作者单位：100853北京，解放军总医院南楼临床部外二科（顾峥峥）， 南楼临床部外一科（孟晓敏） ·144·中华保健医学杂志2012年4月第14卷第2期Chin J Health Care Med，April2012，Vol14，No.2
腹腔镜前列腺癌根治术-Word整理
腹腔镜前列腺癌根治术 主刀：王东（8号手套） 体位：仰卧位，两腿屈曲外展，头低脚高，上肩托，垫头枕，两手放于身体两侧，左手穿动脉，右手建立静脉双通道，其中一通道接延长管。 设备：腔镜设备一套置于患者右侧下方、超声刀、艾尔博电外科工作站（或双极） 布类：（特殊布类）大布类、小布类、盆、疝气包 器械：10mm穿刺器2套、5mm穿刺器1套、进口光纤、气腹管、单极线、10mm镜子（storz）、弯钳2、平钳1、针持1、吸引棒1（国产）、注水棒1、气腹针1、剪刀1、锁扣钳（中号）、电凝钩1、电凝棒1、百克钳1、百克剪1、（或双极一套）、超声刀36号、开腹电刀头、冲洗管 一次性用物：大纱4、小纱10、12号乳胶尿管、注射器50ml、20ml各一、引流袋5个、4、7号慕斯线各一、腔镜套针、镜套、腔镜敷贴5—6个、蕈形尿管24#或26#各两根（剪去头部，作引流管用） 高值：强生2—0八针、中号锁扣夹、强生Y605、三腔硅尿管20号 手术步骤： 1、麻醉完成后，安置体位，消毒铺巾（暴露脐至阴茎），手术 医生
导尿固定于手术台。 2、取脐下缘（A），10mm穿刺器，左髂前上棘与脐连线中外 1／3（B）、中内1/3 ( C )，右髂前上棘与脐连线中内1／3（D）、中外1／3（E）均用12mm一次性穿刺器。 3、于腹膜内间隙注入二氧化碳（15mmHg）,流量15L/min 4、置入手术器械，用超声刀、百克钳打开距膀胱直肠陷窝最 底部上方约2 cm处的腹膜反折弓，游离双侧输精管和精囊腺直至与前列腺的会合处。在前列腺与精囊会合处后方约3 mm，横行切开Denonvillier筋膜，沿前列腺后壁与直肠前间隙分离至前列腺尖部 5、膀胱内注入200ml生理盐水。于脐两侧内侧壁之间做“倒 U”型腹膜切口，进入膀胱前间隙。2—0(八针)可吸收线缝扎阴茎背血管复合体 6、横行切开前列腺周围筋膜，环形切断膀胱颈前壁、两侧和 后缘 7、用超声刀紧贴前列腺包膜切断直至前列腺尖部处理前列腺 侧韧带，并保留神经血管束 8、紧贴前列腺包膜，离断阴茎背血管复合体，游离前列腺尖 部并离断膜部尿道，完整切除前列腺，在前列腺与尿道间露出的尿管上两颗锁扣夹，并剪断尿管，拉出用直钳固定于腹壁 9、用强生Y605可吸收线连续缝合膀胱尿道后壁，间断缝合
前列腺癌根治术后加上后期治疗能活多少年
前列腺癌，是一种比较常见的男性疾病。前列腺癌做完手术以后还能活多长时间呢？这是很多前列腺癌患者想要关注的问题，一些前列腺癌患者总是认为前列腺癌没办法去治疗。这种观点是不正确的，目前治疗前列腺癌的方法还是非常多的。下面一起来了解一下。 目前，治疗前列腺癌的首选方法仍旧是手术治疗，前列腺癌术后生存期主要看是否早期治疗。但大部分肿瘤，早期一般可毫无症状，发现时一般都为中晚期。只有很少一部分患者发现的时候是早期，对于早期患者来说，手术是治疗前列腺癌的首选治疗方法，手术治疗分为根治性手术治疗和姑息性手术治疗，根治性手术切除后患者经过积极的治疗，患者可以获得较长时间的生存期，但是对于癌细胞已经扩散，做了手术切除的患者，术后的巩固治疗是不能少的，以防止复发和转移，对于患者来说术后的复发是患者最怕的，因此巩固治疗是非常重要的，那么前列腺癌术后应该怎么做呢？ 1、选择高蛋白质食物： 吃东西最好选择蛋白质高，脂肪、胆固醇低的，好像各种鱼、虾类。海参有抗癌作用，可以制作海参肉末胡萝卜大米粥食用。鸡蛋每天可以食用1～2个，也可以食用鸭蛋、鹌鹑蛋等。用瘦肉制作的丸子、炖排骨等也可以适量食用。动物肝脏是很好的高蛋白食物，病人每天可食用50克左右，血脂高的病人应限量，同时应搭配绿叶蔬菜一同食用。另外，鸭血、猪血也是理想的高蛋白食物，含有多种维生素和微量元素，可做成汤菜食用。 2、：保证必需脂肪的供给 保证必需脂肪的供给对术后康复也十分必要，选择高蛋白食物时要限制猪肉中的脂肪摄入量，增加深海鱼类、禽肉的供给，因为这些食物含有欧米伽3必需脂肪酸。烹调油可用橄榄油、芝麻油等。 3、中药巩固治疗 前列腺癌患者在术后往往还会有残留的癌细胞，因此对于患者术后为了防止癌细胞扩散和转移，常用中医辅助治疗，中医药具有清热解毒、活血化瘀、扶正固本、软坚散结的功效，能杀伤癌细胞，提高患者的免疫力，增强抵抗力，有效提高手术的成功率。对于中晚期不能手术、放化疗的患者而言，单独采用中医治疗也能起到延长寿命，提高生活质量的作用，如临床上应用广泛的三联平衡疗法受到很多患者欢迎，目前已经帮助了数万例的的癌症患者，重拾了健康。 4、精神饱满，情绪乐观。如精神高度紧张、情绪易于波动、情感上过于脆弱等都会造成食寝不安、身体抗癌能力下降，引起病情的恶化。因此患者需保持乐观的心态，家属也要做好这方面的工作，多于患者进行沟通。 5、进行适当体育锻炼。患者可根据自身体质情况，选择散步、游泳、打太极拳、习剑和慢跑等活动项目，运动量以不感到疲劳为度。 以上就是上文的介绍，希望能帮助到大家，得了前列腺癌大家也没有必要过于害怕，术后做好护理工作，配合中医药的治疗，防止复发和转移，同时保持乐观的心态，能获得较长时间的生存期。
机器人辅助腹腔镜与标准腹腔镜前列腺癌根治 术疗效比较的Meta分析
Asian Case Reports in Surgery 亚洲外科手术病例研究, 2018, 7(3), 17-30 Published Online September 2018 in Hans. https://www.wendangku.net/doc/354692651.html,/journal/acrs https://https://www.wendangku.net/doc/354692651.html,/10.12677/acrs.2018.73004 Comparison of Perioperative and Functional Outcomes between Standard Laparoscopic and Robotic-Assisted Radical Prostatectomy: A Systemic Review and Meta-Analysis Shuchang Huang, Minbo Yan, Wenfei Lian Department of Urology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai Guangdong Received: Nov. 1st, 2018; accepted: Nov. 22nd, 2018; published: Nov. 29th, 2018 Abstract [Objective] The goal of this study was to perform a systemic review and meta-analysis to evaluate the perioperative and functional outcomes between laparoscopic radical prostatectomy (LRP) and robotic-assisted radical prostatectomy (RARP). [Methods] A literature search of EMBASE, MEDLINE, PubMed, and Cochrane Library databases was conducted. We selected randomized con-trolled trials (RCTs) and non-randomized comparative studies (including prospective and retros-pective studies) comparing perioperative and functional outcomes of both LRP and RARP, and meta-analysis was applied using the Review Manager 5.3 software. [Results]Twenty-four studies were identified in the literature search, including 2 RCTs, 7 prospective studies, and 15 retrospec-tive studies. LRP and RARP showed similarity in the operative time, catheterization duration, in-hospital stay, and overall complication rate (P > 0.05). However, blood loss and transfusion rate were lower in RARP (P < 0.05). Moreover, RARP was associated with significantly improved out-comes for continence and potency rates to those of LRP at 3, 6, and 12 months postoperatively (P < 0.05). [Conclusion]RARP was associated with lower blood loss and transfusion rate and much greater functional outcomes in contrast to LRP. Keywords Prostate Cancer, Radical Prostatectomy, Laparoscopy, Robotics, Meta-Analysis 机器人辅助腹腔镜与标准腹腔镜前列腺癌根治术疗效比较的Meta分析 黄书畅，延敏博，练文飞
腹腔镜前列腺癌根治术
腹腔镜前列腺癌根治术 局限性前列腺癌主要指肿瘤局限于前列腺内，未穿透前列腺被膜以及腺外组织，无远处转移。对于这一类前列腺癌，根治性前列腺切除术是最有效的方法。因腹腔镜前列腺癌根治术具有较多优势而越来越广泛地在临床中被应用，本期我们很荣幸地邀请到张骞主任，为广大患者朋友们详细介绍腹腔镜前列腺癌根治术。 ?·腹腔镜前列腺癌根治术的主要手术方法 ?·腹腔镜前列腺癌根治术的手术适应症 ?·腹腔镜前列腺癌根治术的优势 ?·腹腔镜前列腺癌根治术有待改进之处 ?·腹腔镜前列腺癌根治术的回顾及展望 查找专家免费咨询直接通话预约加号 叶定伟复旦大学附属肿瘤医院泌尿外科主任医师得票:252 近期回复:128 张骞北京大学第一医院泌尿外科副主任医师得票:311 近期回复:4 张骞 职称：副主任医师 医院：北京大学第一医院 科室：泌尿外科 o o o 腹腔镜前列腺癌根治术有三种主要术式，即传统的经会阴、经耻骨后及近年蓬勃发展的 腹腔镜前列腺根治性切除术。国内首推耻骨后根治性前列腺切除术和腹腔镜前列腺癌根治术。耻骨后根治性前列腺切除术为传统开放性手术中的一种，具有术野开阔,操作简便易行,可经同一入路完成盆腔淋巴结切除,达到根治目的的优点。腹腔镜手术为近年来蓬勃开展起来的新兴手术方式，它与开放性手术步骤是类似的，都需要完整的切除前列腺并且将尿道和膀胱重建，二者最大的不同在于到达盆底的进入路径以及手术视野。 1、临床上局限性前列腺癌：即可以通过手术达到彻底切除的前列腺癌。 2、年龄：随着年龄的增长，手术合并症的发生率会大幅升高。据此，2010年国际临床操作指南提出，预期寿命在10年及以上的患者推荐选择根治性前列腺癌切除术，以根治性切除肿瘤为目标。 3、一般状况：患者需要具备一定的身体承受能力，即没有严重的合并疾病。这和一般的腔镜手术要求是类似的。 4、手术水平：有经验的术者会给手术带来更好的效果。 5、补救性治疗：对于高剂量外照射治疗、放疗或者化疗后没有远处转移的患者若发现局部复发，经过严格筛选，可以施行补救性的前列腺根治性切除术。 ?腹腔镜前列腺癌根治术的手术时机：经直肠穿刺活检者应等待6～8周、经尿道
人前列腺癌细胞;LNCaP贴壁培养
人前列腺癌细胞；LNCaP贴壁培养 细胞名称：人前列腺癌细胞；LNCaP 形态特性：上皮样；梭形 生长特性：贴壁生长 培养条件：RPMI1640(w/o Hepes)+10%FBS 传代方法：1:3~1:6传代；5~7天1次 冻存条件：细胞冻存液 特征特性： 该细胞由Horoszewicz JS于1977年从一名50岁的明确诊断为转移性前列腺癌的白人男性患者的左锁骨上淋巴结细针穿刺的活体组织中分离建立的。5-α-双氢睾酮可影响该细胞的生长和酸性磷酸酶的产生。该细胞不形成均一的单层而是成簇生长，所以传代的时候要反复吹打形成单个细胞；该细胞贴壁不牢，达不到汇合状态，而且会使培养基迅速变酸；传代后48h内一定要保持培养瓶静止。如果此时挪动培养瓶，会使大部分细胞从瓶底脱落。如果出现此种情况，需要重新孵育24~48h使细胞重新贴壁，细胞贴壁后可更换培养基。 细胞处理方法： 1.细胞在培养瓶中培养至状态良好后灌满培养基运输，获得细胞后用酒精棉球擦拭瓶口消毒，然后在超 净台中操作。 2.如细胞生长至70%-80%，将瓶中的培养基移入无菌瓶中留作培养使用，保留5-8mL培养基在37℃、5% 的CO2的温箱中继续培养。细胞培养至90%-100%后，按要求消化传代。 3.弃去培养基，用无菌PBS或者其他缓冲液清洗细胞2次，加入适量胰蛋白酶消化（EDTA胰酶），待细胞 完全脱壁后加培养基吹打混匀，分瓶培养。 特别注意：（如使用公共实验室或初次接触细胞培养，建议添加双抗培养）
1.我们使用自产培养基及进口血清培养细胞，在您拿回细胞后，如想更换其它品牌培养基，请依照逐次替换的原则，先保留培养瓶中的培养基，多日多次代逐步更换，以减轻对细胞的刺激。 2.如签收时出现培养瓶壁破裂，漏液等情况请及时拍照并联系售后。 3.细胞任何售后问题，均需拍照存档并在2周之内及时联系客服。
腹腔镜前列腺癌根治的临床体会
腹腔镜前列腺癌根治的临床体会 目的分析前列腺癌采用腹腔镜根治术治疗的临床效果。方法选取我院2008年4月～2014年3月接收治的15例前列腺癌患者作为临床研究对象，所有患者均采用腹腔镜前列腺癌根治术治疗，对患者的治疗效果进行观察分析。结果15例患者中，14例患者手术均顺利进行，1例患者因术中出血转为开放手术，手术治疗时间为150～240min，平均手术时间为210min；术中出血量为110～600mL，平均术中出血量为300mL；术后，3例患者出现吻合口漏尿，引流后痊愈。12例有不同程度尿失禁，3例出现吻合口狭窄经尿道扩张后好转。结论前列腺癌患者采用腹腔镜根治手术，具有手术空间大，手术野清晰，术中出血量较少，并发症发生率低，具有较高的安全性和有效性，值得臨床推广应用。 标签：腹腔镜；前列腺癌根治术；并发症；疗效 随着我国人口老龄化趋势的不断发展，人们饮食结构的不断调整，前列腺癌发病率在不断提高。目前，临床中治疗前列腺癌患者主要采用开放手术和腹腔镜前列腺癌根治术治疗，疗效较为确切[1]。我院收治的15例前列腺癌患者给予腹腔镜前列腺癌根治术进行治疗，取得较好疗效，报道如下。 1资料与方法 1.1一般资料选取我院2008年4月～2014年3月接收治疗的15例前列腺癌患者作为临床研究对象，其中，年龄65～78岁，平均年龄（67.2± 2.1）岁；15例患者中，4例肛门指检发现前列腺结节，10例前列腺特异抗原升高（PSA），1例前列腺电切术后3年发现前列腺癌，15例均术前行前列腺穿刺活检和盆腔CT、MRI确诊。本组患者术后病检均无局部淋巴结转移；术前同位素骨扫描未见异常。无严重心、肺等重要脏器疾病。 1.2方法入院后甲硝唑等常规肠道准备；术前晚清洁灌肠，留置导尿，术前半小时常规静脉使用抗生素，本组均行气管内插管全麻，仰卧位，调整手术台，取头低足高位，在脐孔下缘作弧形切口 2.5cm，置入气腹针，腹内压维持在1.7Kpa，腹腔镜引导下，分别在左右髂前上棘内侧和左右腹直肌旁位置插入2个5mm和1个10mm的Trocar建立手术通道。常规行盆腔淋巴结清扫后，超声刀用Monstouris方法分离两侧精囊和前列腺后壁，分离膀胱前壁、扩展Rezius间隙，切开两侧盆筋膜、缝扎耻骨后血管复合体、分别切开膀胱颈前、后壁，分离结扎两侧前列腺血管，尽量保留勃起神经，仔细游离前列腺尖部，适当退出气囊尿管，切断前列腺尖部尿道，可吸收线缝合膀胱颈，膀胱颈成行后与后尿道间断吻合并妥善固定气囊尿管。 2结果 本组15例患者中，14例患者手术均顺利进行，1例因术中出血，手术视野不清中转手术，手术治疗时间为150～240min，平均手术时间为210min；术中
2021年腹腔镜前列腺癌根治术
腹腔镜前列腺癌根治术 欧阳光明（2021.03.07） 主刀：王东（8号手套） 体位：仰卧位，两腿屈曲外展，头低脚高，上肩托，垫头枕，两手放于身体两侧，左手穿动脉，右手建立静脉双通道，其中一通道接延长管。 设备：腔镜设备一套置于患者右侧下方、超声刀、艾尔博电外科工作站（或双极） 布类：（特殊布类）大布类、小布类、盆、疝气包 器械：10mm穿刺器2套、5mm穿刺器1套、进口光纤、气腹管、单极线、10mm镜子（storz）、弯钳2、平钳1、针持1、吸引棒1（国产）、注水棒1、气腹针1、剪刀1、锁扣钳（中号）、 电凝钩1、电凝棒1、百克钳1、百克剪1、（或双极一套）、超声刀36号、开腹电刀头、冲洗管 一次性用物：大纱4、小纱10、12号乳胶尿管、注射器50ml、20ml各一、引流袋5个、4、7号慕斯线各一、腔镜套针、镜套、腔镜敷贴5—6个、蕈形尿管24#或26#各两根（剪去头部，作引流管用） 高值：强生2—0八针、中号锁扣夹、强生Y605、三腔硅尿管20号 手术步骤：
1、麻醉完成后，安置体位，消毒铺巾（暴露脐至阴茎），手术 医生导尿固定于手术台。 2、取脐下缘（A），10mm穿刺器，左髂前上棘与脐连线中外1 ／3（B）、中内1/3 ( C )，右髂前上棘与脐连线中内1／3（D）、中外1／3（E）均用12mm一次性穿刺器。 3、于腹膜内间隙注入二氧化碳（15mmHg）,流量15L/min 4、置入手术器械，用超声刀、百克钳打开距膀胱直肠陷窝最底 部上方约2 cm处的腹膜反折弓，游离双侧输精管和精囊腺直至与前列腺的会合处。在前列腺与精囊会合处后方约3 mm，横行切开Denonvillier筋膜，沿前列腺后壁与直肠前间隙分离至前列腺尖部 5、膀胱内注入200ml生理盐水。于脐两侧内侧壁之间做“倒U” 型腹膜切口，进入膀胱前间隙。2—0(八针)可吸收线缝扎阴茎背血管复合体 6、横行切开前列腺周围筋膜，环形切断膀胱颈前壁、两侧和后 缘 7、用超声刀紧贴前列腺包膜切断直至前列腺尖部处理前列腺侧 韧带，并保留神经血管束 8、紧贴前列腺包膜，离断阴茎背血管复合体，游离前列腺尖部 并离断膜部尿道，完整切除前列腺，在前列腺与尿道间露出的尿管上两颗锁扣夹，并剪断尿管，拉出用直钳固定于腹壁9、用强生Y605可吸收线连续缝合膀胱尿道后壁，间断缝合两侧 壁。洗手护士插入三腔导尿管至膀胱，间断缝合前壁
腹腔镜前列腺癌根治术后出院指导
腹腔镜前列腺癌根治术后出院指导 首先恭喜您可以出院啦！那么出院后吃东西有没有忌口？能运动么？什么时候复查？下面我们来聊聊出院后还需要注意些什么。 一、观察和保护伤口 1.注意观察伤口，如果出现红、肿、热、痛或渗血、渗液请及时就医。 2.伤口愈合之前可用湿毛巾擦洗非手术区域，避免弄湿敷料。一旦敷料弄湿，应及时更换。待伤口完全愈合后方可洗澡。洗澡后应用柔软的干毛巾吸干伤口处的水分，以免损伤伤口处皮肤。 3.伤口上的痂皮应待其软化后自然脱落，不要故意去除。术后 3-4天后可能出现伤口痒的正常反应，不必惊慌。不宜搔抓，不宜用衣物摩擦或以温水烫洗伤口，以免加重痒感或导致伤口感染。这种痒的感觉，以后会自然消失。实在瘙痒难耐，可在医生指导下涂搽消炎抗过敏药物。 二、观察和保护尿管 如果您在出院的时候还留有导尿管，请按照术后要求做好自我护理。 一般在术后1～2周拔管。请遵医嘱按时回医院拔除尿管。 三、合理饮食 宜吃低脂肪、高蛋白、富含维生素、清淡、易消化的食物，如鸡肉、鱼肉、瘦肉、鸡蛋、新鲜的蔬菜和水果，以加强营养、预防便秘。
禁烟禁酒，避免有害物质对身体造成不良影响。 四、日常生活注意事项 1.休息与活动 多注意休息，劳逸结合。出院后病人应以简单的有氧运动为宜，不可过于劳累，每次运动10～20分钟，每天1～2次，并循序渐进逐渐增加运动量。术后3个月内避免剧烈运动，如负重、骑车、登高、跑步等。 2.注意个人卫生 保持会阴部干燥清洁，勤换内裤，以免发生尿路感染。 3.遵医嘱服药 如果医生为您开具了需要在院外服用的药物。您需要遵医嘱按时
服药，不可擅自停药、减药。 4.坚持盆底肌锻炼 术后早期您可能会有不同程度的尿失禁，经6～12个月的盆底肌肉功能锻炼之后多能恢复。 五、定期复查 通常术后6周左右返院复查第1次。如无异常情况，每3月复查1次，2年后每6月复查1次，5年后每年复查1次。 复查项目可能包括：血清前列腺特异性抗原（PSA）、直肠指诊、直肠超声、胸片、盆腔MRI或CT、腹部CT、骨扫描等。注意：病情不同，复查时间和复查项目可能有所区别，具体请听从医生安排。复查时请记得带好您的病历本及检查资料。 六、其他需要及时就医的情况
前列腺癌术后随访流程
前列腺癌根治术后随访计划 武汉同济医院泌尿外科曾晓勇 1.术后一月来门诊第一次复查，需要检测项目：1. PSA； 2.尿常规； 3. B超：肾脏和膀胱，此外向医生报告排尿情况，排尿是否通畅？有无尿失禁？；行保留性神经根治术者报告勃起情况，等等； 2.术后半年内所有患者均需每月定期检查PSA水平；如果PSA 水平稳定降低至< 0.2ng/mL，以后可每三个月查一次PSA，直至PSA再度升高超过0.2ng/mL，或稳定低水平直到术后二年，然后每半年一次PSA； 3.如果术后一个月后PSA检测超过0.2ng/mL，预测有部分肿瘤残留，需要增加辅助内分泌治疗。根据最新国外文献报道，前列腺癌根治术后的肿瘤残留发生率（切缘阳性）高达50%，这类患者均需要术后辅助药物治疗（如内分泌治疗、化疗、或分子靶向治疗、分子免疫治疗）或辅助放疗； 4.如果术后PSA一度下降至0.2ng/mL，又上升至0.2以上，尤其0.5以上，则提示生化复发，需要进一步检查确认是否病理复发，如骨扫描、PET-CT（PSMA-PETCT）等，了解是局部复发还是远处转移，一般需要追加辅助治疗； 5.其他检查：接受内分泌治疗的患者需要查血清睾酮的水平，睾酮水平去势后应低于50ng/mL（1.7mmol/L）；如果接受阿比特
龙或多西他赛等治疗，还应该查血常规、肝肾功能、电解质等。定期复查胸片、肝肾B超，胸腹部CT等，了解有无肿瘤转移。 最后说一句：前列腺癌虽然是恶性肿瘤，但如果治疗得当，都可以获得很长时间的生存和较好的生活质量，甚至不影响患者的自然寿命！应坚持以根治手术为中心的综合治疗，坚持复查和监控，在疾病发展的不同阶段，及时地调整治疗方案，获得最佳的治疗效果。
腹腔镜下前列腺癌根治术的手术配合
腹腔镜下前列腺癌根治术的手术配合 发表时间：2014-04-24T14:38:54.793Z 来源：《中外健康文摘》2013年第44期供稿作者：刘庆兰 [导读] 前列腺癌是常见的男性泌尿生殖系统肿瘤之一，发病率逐年上升。 刘庆兰 (天津医科大学第二医院手术室 300211) 【摘要】目的：探讨腹腔镜下前列腺癌根治术的手术配合方法。方法：总结分析45例采用腹腔镜下前列腺癌根治手术的护理配合。术前充分做好各项检查及准备，手术室护士掌握配合要点，熟悉手术仪器的性能和使用方法，术中密切配合，严密观察病情及完善各项手术护理。结果：手术进展顺利，无一例中转开腹，术后未发生手术并发症，患者术后恢复良好。结论：术前精心准备，术中密切配合，熟练掌握器械使用和维护，是保证手术顺利完成的关键。 【关键词】腹腔镜前列腺癌根治性切除术手术配合 【中图分类号】R737.25 【文献标识码】A 【文章编号】1672-5085（2013）44-0036-02 前列腺癌是常见的男性泌尿生殖系统肿瘤之一，发病率逐年上升。前列腺癌根治术是局限性前列腺癌治愈的最佳方法[1]。由于前列腺周围有许多重要器官和组织。因此，常规采用的开放性前列腺癌根治术创伤大，出血多，并发症发生较高。而腹腔镜下前列腺癌根治术，具有手术切口小、出血少、术后恢复快、病人痛苦小等优点，特别是腹腔镜还具有放大作用，术野清晰，切除病灶和清扫淋巴更彻底，大大减少了术中出血的风险和术后尿失禁等并发症的发生。腹腔镜前列腺癌根治术逐渐成为治疗早期前列腺癌的一种规范手术[2]。2010年12月-一2013年10月。我院对45例病人行腹腔镜下前列腺癌根治性切除术，术后效果满意，现将手术配合介绍如下。 1、临床资料： 本组前列腺癌45例，年龄60～72岁，平均66.5岁。术前行B超引导下前列腺穿刺活检，病理检查证实为前列腺癌。临床分期为：cTlb 6例，cT2a15例，cT2b19例，cT2c5例，平均活检Gleason评分为(5.6±1.2)分，前列腺体积为38～50 m1 (平均45 m1)。盆腔CT和MRI及全身骨扫描未见前列腺外浸润或淋巴结及脏器转移。均在气管插管全麻下，经腹腔镜下行前列腺癌根治术，45例手术均获成功，无1例中转开腹。平均手术时间为5.5 h，平均出血量为350ml。术中配合默契，手术顺利，术后均平安返回病房。 2、手术配合： 2.1 术前准备： 2.1.1 患者准备：因患者年龄较大，手术难度大，风险较高，对腹腔镜的手术缺乏了解和信心，易产生恐惧心理。巡回护士术前1天到病房访视患者，通过观察，阅读病历等方法，掌握患者的病情和生命体征。术前访视针对患者心理进行干预，讲解手术必要性及可行性，讲解腹腔镜手术的特点及优越性，同时耐心解答患者的疑问，做好患者心理疏导，消除患者的紧张和恐惧心理，增强信心，取得信任，并能与医护人员密切配合[3]。 2.1.2 物品准备：备腹腔镜设备系统、超声刀，高压冲洗，负压吸引，术前检查仪器的工作状态，保证所有物品性能良好。备12mm腹腔穿刺器、显影纱布、止血海绵、内镜取物器、3-0可吸收缝线、20F双腔尿管、50ml注射器、腹腔引流管等。另备加热无菌注射用水60～70℃，以供术中预热腹腔镜镜头之雾。器械的准备包括普通开腹器械和腔镜特殊器械，备剖腹器械1套，做好随时转开腹手术的准备。 2.2 巡回护士配合： 2.2.1 建立静脉通道：麻醉前用20 G静脉留置针在上肢建立1条静脉通路，并与术前30min静滴抗生素。麻醉后留置颈内或锁骨下深静脉双腔导管。配合麻醉医生行桡动脉穿刺，并连接各测压装置。 2.2.2 体位护理：全身麻醉后患者先取平卧位，垫高臀部，上肩托。常规消毒铺巾，建立气腹，经腹置入Trocar后，转15℃头低脚高位，以方便手术操作。为防止倾斜过度致患者术中体位滑动，双肩以锁骨为支点用肩托固定。术中密切观察肩托的位置和患者舒适情况，防止倾斜过度患者向头部滑动，引起臂丛神经损伤。 2.2.3 合理摆放物品和仪器：腹腔镜手术所需的贵重仪器品种多，巡回护士必须熟练掌握各种仪器的操作规程及使用注意事项。为方便手术者操作，通常将腹腔镜设备放置于手术床尾，理顺各种导线，避免相互缠绕而影响操作。 2.2.4 密切观察生命体征,调节合适的气腹压力: 前列腺癌根治术在切断耻骨后阴茎背深血管复合体时，出血量较多，术中需密切观察病情及生命体征，严密监测出血量、血氧饱和度，根据血气分析，调节合适的气腹压力[4]。患者年龄较大，一般气腹压力控制在12～ 14mmHg，CO2流量设置为15～30L/min，从低流量逐渐调至高流量，防止气腹压力过高引起高碳酸血症和心律失常等并发症，保证患者生命的安全。 2.3 器械护士配合： 2.3.1 术前与手术医生沟通：掌握手术方式及配合要点，熟悉手术部位的解剖结构、所需的特殊器械物品及术中的注意事项。 2.3.2 切皮前准备：器械护士于20min洗手，清理手术器械台，检查器械完整性，将腹腔镜器械装配好，妥善放置于器械台上，与巡回护士共同清点器械将台上器械摆放有序。 2.3.2 术中仔细观察手术进程：准确传递术者所需的各种器械，及时准备止血纱布。整个手术过程中必须保证腹腔镜镜面清晰，应及时用备好的热无菌注射用水浸泡镜头。及时清除超声刀头上的烧焦组织，确保仪器的正常使用。 2.3.3 术中配合：常规消毒铺巾后，于脐下正中作2cm切口，于左右麦氏点和左右侧脐于髂前上棘连线内1/3处各置入穿刺套管，注入C02，建立气腹。在切断前列腺蒂时传递Lock钳夹闭前列腺蒂并用剪刀剪断前列腺蒂。处理耻骨后血管复合体及前列腺尖时用剪刀。游离前列腺后，将前列腺放入标本袋并置于髂窝。在无张力状态下吻合膀胱颈后壁，精细对合，并将吻合后的膀胱颈前壁与耻骨前列腺韧带缝合。依次传递3-0可吸收缝合线做尿道与膀胱颈连续缝合。吻合完毕，预先插入20 F双腔尿管。待后吻合完毕后经尿管向膀胱内注入120 ml 生理盐水，检查吻合口是否渗漏，明显渗漏者缝合修补。检查手术创面有无渗血，耻骨后置入引流管，排尽腹腔内二氧化碳气体，拔除Troear，清点手术器械，缝合切口。 3、讨论： 3.1高碳酸血症的预防和护理：此手术气腹时间较长，如果患者年龄大，术前合并症多，术中比较容易发生CO2潴留。本组病例中，2例患者在气腹4h后CO2分压超过55mmHg(1mmHg=0.133kPa)，术中应注意检查和避免皮下气肿的发生，一旦发生广泛皮下气肿，应密切
腹腔镜前列腺癌根治术
腹腔镜前列腺癌根治术 Document number：NOCG-YUNOO-BUYTT-UU986-1986UT
腹腔镜前列腺癌根治术 主刀：王东（8号手套） 体位：仰卧位，两腿屈曲外展，头低脚高，上肩托，垫头枕，两手放于身体两侧，左手穿动脉，右手建立静脉双通道，其中一通道接延长管。 设备：腔镜设备一套置于患者右侧下方、超声刀、艾尔博电外科工作站（或双极） 布类：（特殊布类）大布类、小布类、盆、疝气包 器械：10mm穿刺器2套、5mm穿刺器1套、进口光纤、气腹管、单极线、10mm镜子（storz）、弯钳2、平钳1、针持1、吸引棒1（国产）、注水棒1、气腹针1、剪刀1、锁扣钳（中号）、 电凝钩1、电凝棒1、百克钳1、百克剪1、（或双极一套）、超声刀36号、开腹电刀头、冲洗管 一次性用物：大纱4、小纱10、12号乳胶尿管、注射器50ml、20ml各一、引流袋5个、4、7号慕斯线各一、腔镜套针、镜套、腔镜敷贴5—6个、蕈形尿管24#或26#各两根（剪去头部，作引流管用） 高值：强生2—0八针、中号锁扣夹、强生Y605、三腔硅尿管20号 手术步骤：
1、麻醉完成后，安置体位，消毒铺巾（暴露脐至阴茎），手 术医生导尿固定于手术台。 2、取脐下缘（A），10mm穿刺器，左髂前上棘与脐连线中 外1／3（B）、中内1/3(C)，右髂前上棘与脐连线中内1 ／3（D）、中外1／3（E）均用12mm一次性穿刺器。 3、于腹膜内间隙注入二氧化碳（15mmHg）,流量15L/min 4、置入手术器械，用超声刀、百克钳打开距直肠陷窝最底部 上方约2cm处的反折弓，游离双侧输精管和精囊腺直至 与前列腺的会合处。在前列腺与精囊会合处后方约 3mm，横行切开Denonvillier筋膜，沿前列腺后壁与直 肠前间隙分离至前列腺尖部 5、膀胱内注入200ml生理盐水。于脐两侧内侧壁之间做“倒 U”型腹膜切口，进入膀胱前间隙。2—0(八针)可吸收线缝扎阴茎背血管复合体 6、横行切开前列腺周围筋膜，环形切断膀胱颈前壁、两侧和 后缘 7、用超声刀紧贴前列腺包膜切断直至前列腺尖部处理前列腺 侧韧带，并保留神经血管束 8、紧贴前列腺包膜，离断阴茎背血管复合体，游离前列腺尖 部并离断膜部尿道，完整切除前列腺，在前列腺与尿道间露出的尿管上两颗锁扣夹，并剪断尿管，拉出用直钳固定于腹壁
前列腺癌根治性切除术后护理
前列腺癌根治性切除术后护理 目的探讨前列腺癌根治性切除术后的临床护理方法及效果。方法选取我院2015年6月～2016年8月收治的前列腺癌患者中抽取92例作为研究对象。随机分组：对照组46例，采用常规护理；观察组46例，在常规护理的基础上采用术后早期康复护理。比较两组患者的护理效果。结果观察组患者的术后并发症发生率明显低于对照组，生命质量评分明显高于对照组，结果对比，差异有统计学意义（P＜0.05）。结论前列腺癌根治性切除术后对患者实施早期康复护理能够有效降低术后并发症发生率，提高患者的生命质量。 标签：前列腺癌；根治性切除术；护理 前列腺癌是肿瘤科常见的上皮性恶性腫瘤，老年男性70～80岁是其多发群体，致病原因主要为遗传、饮食、性行为等[1]。目前，临床中治疗前列腺癌的方法主要为手术，一般而言，早期前列腺癌患者采用根治性切除术可获得痊愈。然而，根治性切除术对人体组织的损伤较大，术后容易出现各种并发症，而患者的生活质量也相应下降[2]。若要减少术后并发症的发生，提高患者的生活质量，则应在术后对患者实施有效的护理干预。本次研究对前列腺癌根治性切除术的术后护理做了探讨，现报道如下。 1 资料与方法 1.1 一般资料 选取我院2015年6月～2016年8月收治的前列腺癌患者中抽取92例作为研究对象。所有患者均实施根治性切除术。随机将患者分为观察组和对照组，各46例。观察组年龄46～79岁，平均（64.80±5.35）岁；病程1～4年，平均（2.41±1.25）年。对照组年龄47～80岁，平均（65.17±4.52）岁；病程1～4年，平均（2.20±1.19）年。经比较，两组患者的一般资料比较，差异无统计学意义（P>0.05）。 1.2 方法 對照组采用常规护理，包括观察生命体征和病情，配合医生进行抢救，常规给药预防感染，等等。观察组在常规护理的基础上采用术后早期康复护理：（1）尿失禁预防与护理。首先，告诉患者定时排尿的重要性，并指导患者自己按压小腹以促进尿液排出，自主排尿1次/隔3 h。其次，指导患者做肛门、尿道括约肌收缩动作训练，3～4次/d，持续10 min/次。最后，开放尿管1次/隔1～2 h，之后逐渐延长尿管开放的间隔时间，开放1次/2～3 h，使膀胱排空。（2）尿道膀胱吻合口护理。为预防吻合口瘘，护理人员应在术后加强尿管护理，经常检查尿管是否通畅，叮嘱患者做好会阴护理，每日清洁两次，保持会阴部干燥卫生[3]。同时，叮嘱患者在翻身或下床时要保护尿管，防止尿管受压，如果发现尿管引流不畅，则需及时将尿管冲洗干净。
前列腺癌根治术后复发的诊断和治疗
前列腺癌根治术后复发的诊断和治疗 发表时间：2008-10-16 发表者：戴波 (访问人次：3578) 戴波，男，副主任医师，副教授，医学博士。2000年本科毕业于原上海医科大学临床医学专业，2003年6月获得复旦大学肿瘤学硕士学位，2008年6月获得复旦大学肿瘤学博士学位。2003年6月起在复旦大学附属肿瘤医院泌尿外科工作，2006年晋升为主治医师，2010年晋升为副主任医师。长期从事泌尿系统肿瘤的临床诊治与基础研究工作。全面系统地掌握了泌尿系统肿瘤的诊断方法及治疗策略。近年来，在国内外一流学术刊物上以第一作者发表科学论文10余篇，主持或参与多项国家级科研项目，作为第一完成人多次荣获科研奖项。2008年通过全国CUREP（Chinese Urologic Resident Education Program）专业培训并获得证书。2009年1月在国际顶尖的肿瘤治疗中心——美国纽约Memorial Sloan-Kettering Cancer Center （MSKCC）进修学习。2009年7月被评为第四届复旦大学十大医务青年。 前列腺癌根治术是目前治疗临床局限型前列腺癌的标准方法之一，与根治性放疗共同构成前列腺癌两种不同的确切性治疗方法。自1988年起血清PSA检测被广泛应用于临床，在前列腺癌的诊断和治疗中发挥了巨大作用。此后短短几年中，临床前列腺癌的分期构成发生了巨大变化。已有转移的晚期前列腺癌患者比例不断下降，而同期临床局限型前列腺癌患者的比例迅速上升，使越来越多的患者有机会接受前列腺癌根治术或根治性放疗这样的确切性治疗。 随着前列腺癌根治术的广泛开展，使许多临床局限性前列腺癌患者获得了根治和长期生存。随着手术技术的日益成熟，该手术的并发症发生率和死亡率不断下降。但是，临床上仍有约40%的患者在术后5年内发生了生化复发，其中多数为期望生存时间较长的年轻患者。有27-53%的患者最终在术后10年发生肿瘤局部复发或远处转移。临床工作中对此类患者的早期发现、正确评估和规范化治疗，有助于提高前列腺癌患者的总体治疗水平[1-3]。 1 前列腺癌根治术后生化复发（也称PSA复发）的定义 在成功的前列腺癌根治术后，患者的血清PSA水平应在2-4周内下降到0值并一直维持于这一临床检测不到的水平。但是对于将要发生临床复发或转移的患者，其PSA会在肿瘤局部复发或远处转移前6-48个月就开始上升[4]。生化复发是肿瘤继续进展并发生临床复发或转移的前兆。根据Pound等[5]的研究结果，没有患者会在不发生PSA上升的情况下就直接发生临床复发或转移。 从理论上讲，前列腺癌根治术后，患者血清PSA呈非0值即为生化复发。但文献中通常将非0值定义为PSA>0.2ng/ml-0.6ng/ml范围内的某一值。定义生化复发的范围不同会造成对同一数据结果的不同解释。就同一组患者的数据而言，生化复发定义为PSA>0.2ng/ml 和定义为PSA>0.4ng/ml相比，使用前一标准术后5年内患者发生生化复发的相对危险度高出后一标准1.3倍[5]。究竟应该将生化复发定义为哪一具体的数值目前还有争议。目前，欧洲泌尿外科学会（EAU）将血清PSA水平连续两次≥0.2ng/ml 定义为生化复发[6-7]。美国学者Amling等[8]分析了2782例接受了前列腺癌根治术的患者的资料。如分别以0.2ng/ml、0.3ng/ml和0.4ng/ml为界，患者PSA水平进一步上升的比率分别49%、62%和72%。由此可见有半数PSA高于0.2ng/ml的病人其疾病并不进展。所以Amling等[8]认为将生化复发定