前列地尔对兔肝缺血再灌注时肝细胞凋亡的保护作用

目的 探讨前列地尔对兔肝脏缺血再灌注损伤时,有效减少肝细胞凋亡的机制.方法 将健康新西兰兔36只随机分为3组:对照组、缺血再灌注组和前列地尔组,3组分别在再灌注60min和90min时,检测血清谷丙转氨酶(ALT)、谷草转氨酶 (AST)、乳酸脱氢酶(LDH)水平.取肝中叶检测兔诱导型一氧化氮合酶(iNOS)、髓过氧化物酶(MPO)以及bcl-2、bax和Caspase-3蛋白表达;并用原位缺口末端标记法(TUNEL)染色比较各组肝细胞凋亡.结果 与对照组比较,缺血再灌注组和前列地尔组在再灌注后ALT、AST、LDH 水平均大幅上升(P<0.05);但前列地尔组兔在再灌注60、90min时ALT、AST、LDH 水平明显低于缺血再灌注组(P<0.05);与对照组比较,缺血再灌注组肝细胞bcl-2、bax、Caspase-3的表达明显增强;前列地尔组与缺血再灌注组比较表达均减弱,但仍强于对照组.TUNEL 法显示前列地尔组、缺血再灌注组与对照组比较凋亡细胞数增多,前列地尔组与缺血再灌注组比较凋亡细胞数减少;与对照组比较,缺血再灌注组与前列地尔组iNOS 与MPO的活性明显增强,前列地尔组与缺血再灌注组比较,该两者活性明显减弱.结论 前列地尔在肝脏缺血再灌注损伤时能有效地保护肝功能,减少肝细胞的损伤,其作用机制可能是通过减少细胞脂质过氧化,从而降低bcl-2、bax、Caspase-3等凋亡基因的表达.

Abstract：

Objective To study the protective the positive effects of alprostadil Hepatocyte Apoptosis by Liver Ischemia-Reperfusion Injury in rabbits. Methods Thirty-six rabbits were made the model of liver ischemia-reperfusion injury, and randourly divided into three groups:Control group, Ischemia-Reperfusion Injury group and Alprostadil intervention group. The alanine aminotransferase (ALT) , aspartate aminotransferase (AST) , lactate dehydrogenase (LDH) were determined; Each group inducible nitric oxide synthase (iNOS) , myeloperoxidase (MPO) and bcl-2, bax, Caspase-3 and apoptosis of the hepatocyte by TUNEL were assayed at 60 and 90 min after reperfusion. Results The ALT, AST, LDH concentration in plasma in Ischemia-Reperfusion Injury group and Alprostadil intervention group were increased obviously at 60, 90 min after reperfusion and it was significantly higher than that in the Control group in the same time point (P<0.05). And the ALT, AST, LDH concentration in plasma in Alprostadil intervention group was significantly lower than that in the in Ischemia-Reperfusion Injury group in the same time point (P<0.05). The level of bcl-2, bax, Caspase-3 in the liver tissue in the Control group was smaller, but the obvious increase of the expression those was found in the Ischemia-Reperfusion Injury group and Alprostadil intervention group. Compared with those in the Ischemia-Reperfusion Injury group group, the expression of bcl-2, bax, Caspase-3 in the Alprostadil intervention group werw obviously smaller (P<0.05). The contents of iNOS and MPO in liver tissue in the Ischemia-Reperfusion Injury group and Alprostadil intervention group were significantly higher than that in the Control group (P<0.05). Conclusion Alprostadil could be used to protect liver ischemia-reperfusion injury, it could decrease oxygen free radicals generation, inhibit neutrophils aggregating and activating in the liver, thereby inhibiting expression of bcl-2, bax, Caspase-3.     

血小板激活因子拮抗剂E5880在肝切除时对肝脏缺血再灌注损伤的保护作用

目的探讨血小板激活因子（platelet—activating factor，PAF）拮抗剂E5880在肝脏血流完全阻断下行70％肝切除术中的肝脏保护作用。方法实验用家兔16只，分成2组。A组：术前无任何预处理，在Pringle法阻断肝脏血流20min下行70％肝切除；B组：术前用E5880（0．3mg／kg）行预处理，在Pringle法阻断肝脏血流20min下行70％肝切除。肝脏再灌注后评估两组动物肝脏功能。结果B组7d存活率较A组显著提高（38％vs0，P〈0．05）；肝脏再灌注1h和4h时，B组血清AST、ALT、mAST、LDH的升高明显被抑制；B组门静脉压和肝脏能荷较A组有明显改善；A、B组肝动脉和门静脉血液中内皮素-1水平均明显升高。B组的肝脏白细胞浸润明显减少。结论术前使用E5880预处理，可以保护在Pringle法阻断肝脏血流20min下行70％肝切除术后肝脏功能。     

前列腺素E_1对肝切除术后肝脏保护作用的临床研究

目的 探讨肝切除术后前列腺素E_1(prostaglandin E_1,PGE_1)对肝脏的保护作用.方法 采用随机对照的方法将82例肝切除病例分为对照组(41例)和PGE_1治疗组(41例,即在对照组治疗的基础上加用PGE_1脂微球载体治疗),观察住院天数、术前后各项指标以及术后3 d内尿量和腹腔引流量的变化.结果 PGE_1治疗组患者较对照组的住院天数明显缩短,中位天数为22 d,明显少于对照组的26 d;术后丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、总胆红素(TBIL)、白蛋白(ALB)的恢复也较对照组显著,术后3 d内的尿量明显增多,腹腔引流量则显著减少.而凝血酶原时间(PT)未见明显改变.结论 PGE_1能有效改善肝切除术后肝功能,降低胆红素水平,并减少术后腹水的形成,缩短住院天数,而对凝血功能无明显影响,用于肝切除术后的保护是安全的.     

前列腺素E1和重组人生长激素对肝缺血-再灌注损伤的保护作用

我们用兔肝脏缺血 再灌注损伤及肝切除模型 ,采用前列腺素Ｅ1 (ＰＧＥ1 )和重组人生长激素 (ｒｈＧＨ)单独及联合用药的方法 ,探索减轻肝脏缺血 再灌注损伤的新方法。一、材料和方法1 .动物及分组 :健康大耳白兔 48只 ,3 %戊巴比妥钠 (30ｍｇ/ｋｇ体重 )静脉注入麻醉 ,阻断第一肝门 40ｍｉｎ时切除左肝外叶 ,45ｍｉｎ后解除阻断。实验动物随机等分为 4组 :Ａ组 (对照组 ,1 2只) ,缺血前后静脉滴注生理盐水 (ＮＳ)0 .5ｍｌ·ｋｇ- 1 ·ｍｉｎ- 1 ;Ｂ组 (ＰＧＥ1 组 ,1 2只) ,缺血前后静脉滴注ＰＧＥ1 0 .5μｇ·ｋｇ- 1 ·ｍｉｎ- 1 ;Ｃ组 (…     

缺血预处理对肝大部切除术中残肝缺血再灌注损伤的保护作用

目的 观察缺血预处理对大鼠肝大部切除术中残肝缺血再灌注损伤的保护作用。方法 健康的雌性SD大鼠随机分为3组：即单纯肝叶切除组（PH组）、缺血再灌注损伤状态下肝叶切除组（IR组）及缺血预处理组（IP组）。分别取术前及术后0．5、6、12、24、48h等时间点，应用全自动生化分析仪检测血清ALT、AST含量，通过免疫组织化学法检测残肝组织中Ki67和Cyclin D1表达变化，采用放免法检测血清中透明质酸（HA）含量。结果 IP组术后24h内各检测点的AST和ALT值明显高于PH组和IR组（P〈0．05）。术后早期IP组大鼠的血清HA表达量明显高于PH组和IR组（P〈0．05）。PH组大鼠肝细胞Ki67和Cyclin D1表达在术后24h达到峰值，并且明显高于IR组和IP组大鼠（P〈0．05）。其中IP组大鼠术后Ki67和Cyclin D1表达量降低地最显著。结论 在合并肝组织大部缺失时，缺血预处理对残留肝组织的缺血再灌注损伤的保护效应消失，它损害了大鼠残肝再生功能。     

前列地尔对兔肾缺血再灌注时细胞凋亡的保护作用

目的 观察前列地尔对兔肾缺血再灌注损伤时肾小管上皮细胞凋亡的保护作用.方法 建立兔肾缺血再灌注损伤动物模型,将实验兔随机分为3组:即对照组、缺血再灌注组和前列地尔组,每组10只.检测兔血清肌苷(Cr)、尿素氮(BUN)浓度及肾组织中丙二醛(MDA)、超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)含量及肾组织中凋亡细胞.结果 与对照组比较,缺血再灌注组和前列地尔组在再灌注后Cr、BUN水平均大幅度上升(P＜0.05);但前列地尔组动物在再灌注60min后Cr水平(231.32±17.57)μmol/L明显低于缺血再灌注组(390.61±20.42)μmol/L(P＜0.05);肾小管上皮细胞bcl-2、bax、Caspase-3表达与对照组比较,缺血再灌注组明显增强(P＜0.05);前列地尔组与缺血再灌注组比较表达减弱,但仍强于对照组(P＜0.05).前列地尔组、缺血再灌注组与对照组比较凋亡细胞数增多,前列地尔组与缺血再灌注组比较凋亡细胞数减少.MDA、SOD与MPO的活性与对照组比较,缺血再灌注组与前列地尔组明显增强(P＜0.05);前列地尔组与缺血再灌注组比较,该两者活性明显减弱(P＜0.05).结论 前列地尔在肾脏缺血再灌注损伤时能有效的保护肾功能其作用机制可能是通过减少细胞脂质过氧化,从而降低bcl-2、bax、Caspase-3等凋亡基因的表达.

Abstract：

Objective To study the alprostadil effects of alprostadil on apoptosis by renal ischemia-reperfusion injury (IR[) in rabbits. Methods The rabbit IRI models were made, and randourly divided into three groups: control group, IR[group and prostavasin intervention group. The creatinine (Ct) and blood urea nitrogen (BUN) were determined. Malondialdehyde ( MDA), superoxide dismutase (SOD),myeloperoxidase ( MPO), bcl-2, bax, Caspase-3 and apoptosis were assayed at 60 min after reperfusion.Results The Cr and BUN levels in plasma in IRI group and Prostavasin intervention group were increased obviously after reperfusion. The Cr levels at 60 min after repeffusion in alprostadil intervention group (231.32 + 17. 57 ) μmol/L were significantly lower than in IRI group ( 390. 61 ± 20. 42 ) μ mol/L, ( P ＜0. 05 ). The levels of bcl-2, bax, Caspase-3 in the renal tissue in IRI group were significantly higher than in control group ( P ＜ 0. 05 ), and those in alprostadil intervention group were lower than in IRI group, but markedly higher than in control group (P ＜ 0. 05 ). The number of apoptotic cells in alprostadil intervention group and IRI group was increased as compared with control group, and that in alprostadil intervention group was reduced as compared with IRI group. The contents of MDA, SOD and MPO in renal tissue of IRI group and Prostavasin intervention group were significantly higher than in control group ( P ＜ 0. 05 ), and those in IRI group were significantly lower than in alprostadil intervention group (P ＜0. 05 ). Conclusion Alprostadil could be used to protect renal ischemia-reperfusion injury probably by decreasing oxygen free radicals generation, inhibiting neutrophils aggregating and activating in the renal tissues, thereby inhibiting the expression of bcl-2, bax, Caspase-3.     

亚低温对肝缺血再灌注损伤的保护作用

目的　探讨亚低温对肝缺血再灌注损伤的保护作用机制。方法　将 18只犬随机分为 3组 :非缺血对照组 (n =6 )、缺血再灌注组 (n =6 )和亚低温处理组 (肝周充填碎冰块造成肝脏亚低温 ,n =6 )。对各组肝上下腔静脉血进行谷丙转氨酶 (ALT)、谷草转氨酶(AST)、乳酸脱氢酶 (LHD )以及丙二醛 (MDA)和超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT)、谷胱甘肽过氧化酶 (GSH PX)活性及总抗氧化 (TAX )能力测定。结果　全肝缺血再灌注后ALT ,AST ,LDH和MDA含量明显上升 (P <0 .0 1) ,SOD ,CAT ,GSH PX活性及TAX能力明显下降 (P <0 .0 1) ;而亚低温处理组与缺血再灌注组比较 ,ALT ,AST ,LDH和MDA含量明显下降 (P <0 .0 1) ,SOD ,CAT ,GSH PX活性及TAX能力明显上升 (P <0 .0 1,P <0 .0 5 )。结论　亚低温能增强肝组织自身抗氧化能力 ,减轻肝缺血再灌注后氧自由基对肝脏的损伤。     

高渗盐水对肝脏缺血再灌注损伤保护作用的临床研究

目的:观察高渗盐水对肝部分切除术中常温下肝脏缺血再灌注损伤的保护作用.方法:60例择期行肝部分切除术的患者,ASA Ⅰ～Ⅱ级,随机分为无肝门阻断组(NPR组)、肝门阻断组(PR)和高渗盐水预处理的肝门阻断组(HS组),每组20例.患者均采用硬膜外复合全身麻醉.NPR组不进行肝门阻断,PR组在肝门阻断前5 min输入生理盐水,HS组在肝门阻断前5 min静脉输入7.5%高渗盐水.分别于术前和肝部分切除后3、15、30 min及2 h抽取肘静脉血行中性粒细胞(PMN)计数,于术后24和48h抽取肘静脉血检测肝功能;在肝部分切除前及切除后30 min取肝组织检测髓过氧化物酶(myeloper-oxidase,MPO)含量.结果:NPR组在肝部分切除后血中性粒细胞计数及肝组织中MPO浓度无变化,但PR组和HS组PMN显著降低(P<0.05),肝组织中MPO浓度显著升高(P<0.05),且PR组变化更为显著(P<0.05);术后3组患者的血浆ALT均升高,PR组升高最为明显,显著高于其他两组(P<0.05).结论:7.5%高渗盐水预处理对常温下肝脏的缺血再灌注损伤有显著保护作用,其机制可能与减少PMN在肝组织内的聚集有关.     

大鼠部分肝缺血再灌注损伤后切除对肝再生的影响

目的 观察大鼠部分肝缺血再灌注损伤后切除对残肝再生的影响.方法 将75只健康雄性SD大鼠随机分为5组:肝脏左叶和中叶(约占全肝70%)切除组(Control组)、肝脏左叶和中叶缺血10min再灌注30min后切除组(I10R30组)、类推得到I60R30组、I90R30组、I90R60组.术后6、12、24h等时间点,测定再生肝重量(RLW);自动生化分析仪检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)含量;酶联免疫吸附试验(ELISA)检测血清肿瘤坏死因子(TNF)-α含量;通过免疫组织化学法检测残肝增殖细胞核抗原(Ki-67)表达.结果 术后12h,I60R30、I90R30和I90R60组RLW值分别为(1.80±0.03)%、(1.82±0.10)%、(1.87±0.05)%;Ki-67值分别为(58.35±2.18)%、(59.73±3.06)%、(62.65±2.24)%,均明显高于对照组(P<0.05).缺血再灌注干预各组ALT和AST明显高于对照组(P<0.05).术后6h和12h,I60R30、I90R30和I90R60组TNF-α明显高于对照组(P<0.05).结论 大鼠即将被切除的肝脏先缺血再灌注后切除,对残肝再生具有促进作用;诱导产生的TNF-α表达量增多是促进肝再生的原因之一.

Abstract：

Objective To investigate the effects of ischemia reperfusion injury before partial hepatectomy on liver regeneration in rats. Methods Seventy-five male healthy SD rats were randomly classified into 5 groups: group control, in which rats were only subjected to 70% hepatectomy; group I10R30, 70% liver hepatectomy after 10 min of ischemia and 30 min of reperfusion in the resected liver; By analogy, group I60R30, group I90R30 and group I90R60 were constructed. At 6th, 12th and 24th h after operation, RLW was determined; serum alanine aminotransferase (ALT) and aspartate transaminase (AST) activities were measured by using autoanalyzer; the levels of serum tumor necrosis factor (TNF)-α were determined by ELISA and the expression level of Ki-67 was detected by using immunohistochemical methods in the residual liver tissues. Results At 12th h after partial hepatectomy, the rate of RLW in group I60R30, group I90R30 and group I90R60 was (1.80±0.03)%, (1.82±0.10)%, (1.87±0.05)% respectively; the rate of Ki-67 was (58.35±2.18)%, (59.73±3.06)%, (62.65±2.24)% respectively, which was significantly higher than that in the group control (P<0.05). The levels of ALT and AST in rats with ischemia reperfusion injury were higher than in the group control (P<0.05). At 6th h and 12th h after operation, the expression levels of TNF-α in groups I60R30, I90R30 and I90R60 were significantly higher than those in the group control (P<0.05). Conclusion Ischemia reperfusion injury in the resected liver before partial hepatectomy could improve liver regeneration of the remnant liver in rats. The high expression of induced TNF-α may be one of the reasons.     

前列腺素E1对大鼠肝脏缺血再灌注损伤的保护作用

目的 探讨前列腺素E1（PGE1）对肝脏 因再灌注损伤的保护作用。方法 制作常温下大鼠部分肝叶缺血再灌注模型，于缺血前经门静脉给予PGE1，45min后恢复血流灌注，并于1h后取门静脉血测定血清谷草转氨酶（GOT）、谷丙转氨酶（GPT）、乳酸脱氢酶（LDH）、肿瘤坏死因子－α（TNF－α）及内皮素1（ET－1），同时取缺血肝叶行病理组织学检查。结果 缺血再灌注组GOT、GPT、LDH及TNF－α和ET－1均明显高于正常对照组，PGE1组则明显低于缺血再灌注组。PGE1组的肝脏病理组织学改变明显轻于缺血再灌注组，并接近正常对照组。结论 PGE1对肝缺血再灌注具有保护作用。     

丙泊酚靶控输注用于肝脏部分切除术的准确性

目的评价丙泊酚靶控输注(TCI)静脉全麻复合硬膜外阻滞用于肝癌行肝脏部分切除术Diprifusor TCI系统的执行情况。方法选择24例择期手术患者,根据手术种类的不同分为肝脏手术组(H组)和普通上腹部手术组(C组),每组12例。以芬太尼4μg/kg、TCI丙泊酚3μg/ml诱导,麻醉维持予丙泊酚TCI复合硬膜外阻滞。观察麻醉期间HR、MAP、脑电双频指数(BIS)、听觉诱发电位指数(AAI)的变化,并抽取动脉血检测丙泊酚的血药浓度。采用执行误差(PE)中位数(MDPE)、PE绝对值中位数(MDAPE)、摆动度(wobble)评价Diprifusor TCI系统执行情况。结果两组麻醉期间的HR、MAP、BIS、AAI、PE、MDPE、MDAPE、wobble比较差异无统计学意义。Dipri-fosor TCI系统总的PE、MDPE、MDAPE、wobble分别为15.43%、11.93%、17.89%、13.09%。结论丙泊酚Diprifusor TCI系统能安全有效地用于全麻复合硬膜外阻滞的肝脏部分切除术患者。     

预先区域性血流阻断在肝脏肿瘤切除术中的应用

目的 探讨预先区域性血流阻断在肝脏肿瘤切除术中的作用.方法 28例肝肿瘤患者采用预先区域性血流阻断技术行肿瘤切除(阻断组),24例采用常规肝肿瘤切除患者(对照组).术前两组患者肝功能Child-Pugh评分均为A级.阻断组术中采用血流阻断针在B超配合下将阻断带置人肿瘤周围肝实质中阻断肿瘤的血流,对照组采用第一肝门阻断法切除肿瘤.结果 阻断组出血量、麻醉时间及术后住院天数分别为(340±92)ml,(98.4±25.0)min,(10.2±2.3)d;对照组为(620±124)ml,(135.8±47.5)min,(16.5±5.1)d,两组比较差异有统计学意义(分别f=9.222,9.328,5.875,均P<0.01).术后第2天阻断组和对照组ALT分别为(378.4±35.2)U/L,(539.2±115)U/L(t=7.012,P<0.01),TBIL(37.5±11.2)mmol/L,(51.8±29)mmol/L(t=8.818,P<0.01),PT(17.4±2.4)sec,(20.4±2.8)see(t=4.16,P<0.01).术后第7天阻断组和对照组ALT分别为(57.1±15.5)U/L,(98.1±21.2)U/L,TBIL(25.4±4)mmol/L,(46.3±13)mmol/L.PT(13.2±4.2)sec,(15.7±2.2)sec,两组相比差异有统计学意义(分别t=8.039,8.085,2.621,均P<0.01).结论 预先区域性肝血流阻断术能较好控制肝癌术中出血有利于术后肝功能恢复.     

清创性肝切除联合选择性向肝血流阻断治疗严重肝外伤

目的 探讨清创性肝切除联合选择性入肝血流阻断对严重肝外伤手术治疗价值.方法 总结清创性肝切除术联合选择性入肝血流阻断治疗严重肝外伤55例的临床病例资料,其中肝外伤Ⅲ级20例,Ⅳ级20例,Ⅴ级15例,伴肝周大血管损伤14例,合并其他伤35例.附加手术:肝间断缝合修补术7例,肝周纱布填塞3例,下腔静脉修补术5例,肝静脉修补术5例,肝静脉缝扎术4例,肝固有动脉结扎2例.其余患者开颅清创3例,胆囊切除6例,胆总管T管引流4例,脾切除术5例,胰体尾部切除2例,左肾切除术1例,胸腔闭式引流9例,小肠部分切除或修补4例,胃修补1例.结果 全组救治成功47例.术后并发症19例(34.5％),其中凝血功能障碍1例,腹腔内出血2例,肠梗阻1例,肝、肾功能不全4例,腹腔感染3例,伤口感染2例,肺部感染4例,胸腔积液10例,均经治疗痊愈出院.死亡8例(14.5％),死亡原因:失血性休克3例,重型颅脑伤1例;重型颅脑伤合并胃、小肠多处破裂1例,感染性休克1例,多器官功能衰竭2例.结论 清创性肝切除联合选择性入肝血流阻断是严重肝外伤手术救治的较好方法.     

肝缺血预处理在肝切除术中应用价值的随机对照研究

目的 探讨缺血预处理在肝切除术中的I临床应用价值.方法 采用前瞻性随机双盲对照的研究方法将安徽医科大学第一附属医院肝胆外科2004年12月至2006年6月收治的48例肝切除患者随机分成两组:预处理组和对照组,每组24例.预处理组采用阻断入肝血流5 min,开放5 min的预处理方式,两组切肝时均按常规肝门阻断法(Pringle法).比较两组术后第1、3、7天肝功能变化情况,以及术后并发症发生率、围手术期病死率及总住院天数.结果 预处理组中肝门阻断时间5～80 min,平均31 min;住院天数13～50 d,平均20 d.对照组中肝门阻断时间10～60 min,平均27 min;住院天数10～33 d,平均17 d.除预处理组中有1例术后3个月死于慢性肝功能衰竭外,余47例均恢复良好.两组术后第1、3、7天丙氨酸转氨酶、天冬氨酸转氨酶、总胆红素、白蛋白的变化均无统计学意义(P>0.05).结论 应用阻断入肝血流5 min的预处理方法无助于肝切除术后患者肝功能的恢复.     

乌司他丁对部分肝切除术后肝功能的保护作用

目的探讨乌司他丁对部分肝切除术后肝功能的保护作用。方法选取2012年3月-2015年2月肝外科中心收治的择期部分肝切除术患者54例(含7例脱落病例),采用随机数表法将患者分为对照组和观察组各27例,剔除脱落病例,观察组最终纳入25例,对照组最终纳入22例,术前1 d及术后1、3、5 d检测肝功能指标、炎性因子、T淋巴细胞及氧化应激指标。结果两组术后1、3、5 d谷丙转氨酶(ALT)、谷草转氨酶(AST)、总胆红素(TBIL)、肿瘤细胞因子α(TNF-α)、白介素-6(IL-6)、C反应蛋白(CRP)、高迁移率蛋白-1(HMGB-1)、丙二醛(MDA)均明显上升,超氧化物歧化酶(SOD)明显下降,与术前1d相比差异明显(P0.05),观察组术后3、5 d ALT、AST、TBIL、TNF-α、IL-6、CRP、HMGB1、MDA上升幅度明显低于对照组,SOD下降幅度高于对照组(P0.05)。两组术后1 d CD_4~+、CD_4~+/CD_8~+明显低于术前1 d(P0.05),术后3、5 d较术后1 d相比明显上升,但与术前1 d对比无差异(P0.05);观察组和对照组不同时间点组间对比无明显差异(P0.05)。结论乌司他丁能下调部分肝切除术后患者炎性因子水平,抑制氧化应激反应,保护肝功能。     

异甘草酸镁对肝硬化大鼠肝部分切除术后肝功能及肝再生的影响

目的 研究异甘草酸镁对肝硬化大鼠部分肝切除术后肝功能和肝再生的影响.方法 45只肝硬化Wistar大鼠行2/3肝部分切除,并随机分为对照组(A组)、治疗组(B组)、术前3 d治疗组(C组).手术当天起,B组给予腹腔注射异甘草酸镁(60mg·kg-1·d-1),A组给予同等剂量生理盐水,C组在手术前3 d即给药(60 mg·kg-1·d-1).各组大鼠分别于术后1、2、7 d处死,检测肝功、血清肝细胞生长因子(HGF)及磷脂酶A2(PLA2)、5-溴脱氧尿苷(BrdU)标记指数、肝再生率.结果 A组在术后第1天,BrdU标记指数及HGF均低于C组(分别t=2.831,3.427,均P＜0.05),而PLA2高于B、C组(分别t=2.794,2.902,均P＜0.05);在术后第2天A组BrdU标记指数均低于B、C组(分别t=2.736,3.083,均P＜0.05),HGF水平与其他两组比较,差异均无统计学意义,PLA2仍高于B、C组(分别t=2.794,2.902,均P＜0.05);A组术后第1、2天ALT、AST、TP水平及肝再生率与B、C组比较,差异均无统计学意义;术后第7天A组AST高于其他两组(A组与B组比较t=4.508,P＜0.05;A组与C组比较t=2.967,P＜0.05),TP水平及肝再生率则均低于B、C组(TP:A组与B组比较t=2.838,P＜0.05;A组与C组比较t=2.743,P＜0.05);肝再生率:(A组与B组比较t=3.316,P＜0.05;A组与C组比较t=4.093,P＜0.05),而BrdU标记指数、HGF、PLA2三组间比较,差异均无统计学意义.B组术后第1天BrdU标记指数及HGF均低于C组(t=2.831,P＜0.05;t=2.836,P＜0.05).结论 异甘草酸镁可降低肝硬化大鼠部分肝切除术后转氨酶水平,改善肝脏功能,促进肝细胞增生.     

Changes in liver blood flow after hepatectomy in conscious dogs

Hepatic circulation after hepatectomy was investigated in conscious dogs under fasting and feeding conditions. After a 40% hepatectomy, both the hepatic arterial and portal blood flow were measured simultaneously using ultrasonic transit time flowmeters. During fasting, the total hepatic blood flow (i.e., the sum of arterial and portal blood flow) changed in a biphasic pattern after hepatectomy. The first peak (517.9±42.7 ml/min; 130.1% of preoperative flow) was seen on the 1st postoperative day (POD) and the second peak (444.8±25.6 ml/min; 112.7% of preoperative flow) occurred on the 7th POD. The portal flow demonstrated the same biphasic changes as the total hepatic flow, although the hepatic arterial flow showed only the first peak. A heart rate analysis suggested that the first peak was probably due to hyperdynamic circulatory conditions, as has been previously reported. In addition, the existence of the second peak was established by the present study. The postprandial hepatic blood flow decreased during the first 2 weeks postoperatively, but exceeded the presurgical levels on PODs 21 and 28.     

再灌注初期控制性降压对肝叶切除术病人肝缺血再灌注损伤的影响

目的 评价再灌注初期控制性降压对肝叶切除术病人肝缺血再灌注损伤的影响.方法 择期行肝叶切除术病人40例,性别不限,年龄30～60岁,体重40～70kg,ASA分级Ⅱ或Ⅲ级,将病人按分层随机方法分为2组(n=20),对照组(C组)开放肝门后10 min期间维持MAP 75～100mm Hg,控制性降压组(H组)于开放肝门前2 min开始静脉输注硝酸甘油3～6μg·kg-1·min-1实施控制性降压,再灌注10 min期间维持MAP 60～70 mm Hg.分别于缺血前(基础状态)、缺血15 min和再灌注25min时采集静脉血样,测定血浆内皮素(ET)、一氧化氮(NO)、TNF-α和IL-1的浓度.结果 与基础值比较,两组缺血15 min和再灌注25min时血浆ET、TNF-α和IL-1的浓度升高,血浆N0浓度降低(P＜0.05);与C组比较,H组再灌注25min时血浆ET、TNF-α和IL-1的浓度降低,血浆NO浓度升高(P＜0.05).结论 再灌注初期控制性降压10 min可减轻肝叶切除术病人肝缺血再灌注损伤,其机制与调节肝窦内皮细胞ET和NO的平衡及抑制炎性反应有关.

Abstract：

Objective To evaluate the effect of controlled hypotension at the beginning of reperfusion on ischemia-reperfusion (I/R) injury of the liver in patients undergoing hepatectomy. Methods Forty ASA Ⅱ or Ⅲ patients aged 30-60 yr weighing 40-70 kg undergoing elective partial hepatectomy for liver cancer were randomly divided into 2 groups ( n = 20 each): group C normal BP and group H controlled hypotension. Hepatic portal was occluded during operation. In group C normal BP was maintained during reperfusion while in group H controlled hypotension (MAP was maintained at 60-70 mm Hg) was performed for 10 min since the beginning of reperfusion.Venous blood samples were taken before hepatic ischemia (T0 ,baseline) and at 15 min of ischemia (T1) and 25 min of reperfnsion (T2 ) for determination of plasma endothelin (ET), nitric oxide(NO), TNF-α and IL-1 concentrations. Results I/R of the liver led to significant increase in plasma ET, TNF-α and IL-1 concentrations and decrease in plasma NO concentration at T1,2 as compared with the baseline values at T0 in both groups. Plasma ET,TNF-α and IL- 1 concentrations were significantly lower while plasma NO concentration was significantly higher at T2 in group H than in group C. Conclusion Ten minutes controlled hypotension in the initial stage of reperfusion can attenuate I/R-induced injury to the liver in patients undergoing hepatectomy by balancing ET with NO and inhibiting inflammation response.     

前列地尔促进移植肝功能早期恢复的临床研究

目的　探讨前列地尔对术后早期移植肝功能恢复的影响。方法　对 6例肝移植患者从术中开始通过中心深静脉用微量泵给予前列地尔 (治疗组 ) ,术后同法持续 2 4h给予 ,拔除中心静脉插管后通过外周静脉缓慢输注 ,直至术后 2 0d ;另有 4例除不用前列地尔外 (对照组 ) ,其余处理同治疗组。观察两组患者术后 2 1d内的血清丙氨酸转氨酶 (ALT)、天冬氨酸转氨酶 (AST)、总胆红素 (TBil)和直接胆红素 (DBil)水平 ,记录胆汁引流量 ;记录各例术后在重症监护病房的留置时间。结果　术后第 1d两组患者的ALT和AST水平均显著升高 ,但治疗组显著低于对照组 (P <0 .0 1) ,3～ 5d后前述指标均迅速恢复至正常水平 ;两个组术后血清TBil和DBil均开始缓慢升高 ,但治疗组的水平明显低于对照组 (P <0 .0 5 ) ,且升高持续时间也短于对照组 (P <0 .0 5 ) ;治疗组的胆汁引流量显著多于对照组 (P <0 .0 5 ) ,需要重症监护的时间显著短于对照组 (P <0 .0 1)。结论　术后早期应用前列地尔对促进移植肝功能的早期恢复有积极意义。