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目前我国是世界上尚未通过脑死亡法的少数国家之一。经过几十年的努力,我国肝脏移植已经取得了很大的成绩,但因为我国没有实行脑死亡法,供肝主要来源于心脏死亡的供体,造成供肝质量较差,导致我国肝脏移植后的疗效不如国际先进水平。实施脑死亡法必将大大促进我国肝脏移植水平的提高。 相似文献
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目的总结并探讨脑死亡无偿器官捐献肝脏移植在我国临床实施的可行性.方法昆明市第一人民医院于2011年12月至2012年1月期间共完成2例脑死亡无偿器官捐献工作.2例供体确诊为脑死亡,应用机械通气、血管活性药物等治疗维持供体器官灌注.受体1男性,术前诊断乙肝后性肝硬化,肝功能失代偿,child-pugh C级,MELD评分29分;受体2男性,术前诊断乙肝后性肝硬化,原发性肝癌,child-pugh C级,MELD评分26分.结果 2例脑死亡供体均顺利无偿捐献肝脏,2例受体均顺利接受肝脏移植手术并康复出院,目前随访移植肝功能良好.结论脑死亡无偿器官捐献肝脏移植的临床实施顺利,可以在我国逐渐推广实行,对缓解我国目前器官短缺状况起到相当重要的作用. 相似文献
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目的观察脑死亡(brain death,BD)肺移植供体吸入一氧化碳(carbon monoxide,CO)对移植肺细胞凋亡的影响。方法将24只大鼠随机分为3组,对照组(sham组)供体鼠颅内置入Fogarty导管,但不膨胀前端球囊;脑死亡组(BD组)和脑死亡CO治疗组(BDCO组)供体鼠颅内置入Fogarty导管,并膨胀前端球囊建立BD模型。sham组和BD组吸入氧气浓度为40%的氧氮混合气150 min,BDCO组在开始BD诱导后30 min,确认BD后,吸入氧气浓度为40%的氧氮混合气和250 ppm的CO2 h。然后进行肺移植,移植后2 h取移植肺组织切片进行TUNEL染色观察移植肺中细胞凋亡情况,使用RT-PCR和免疫组化技术观察Caspase-3 mRNA和蛋白表达情况。使用免疫组化评分(immunohistoche micas scores,IHS)对细胞凋亡和Caspase-3蛋白表达进行评估。结果BD组细胞凋亡程度,Caspase-3蛋白和mRNA表达显著高于sham组(P0.05),BDCO组与BD组相比,上述指标显著降低(P0.05)。结论供体BD过程增加了移植肺细胞凋亡比率,BD供体吸入CO对移植肺再灌注后细胞凋亡有拮抗效应。 相似文献
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目的 观察冬虫夏草浸出液合用硫唑嘌呤对大鼠减体积1/2肝脏移植后免疫调节功能的影响.方法 80只大鼠,随机分为空白对照组、模型组、硫唑嘌呤组、冬虫夏草组,采用改良双袖套法进行1/2大鼠同种异体减体积原位肝脏移植,术后硫唑嘌呤组用硫唑嘌呤稀释溶液灌胃1.0 mg/(kg·d)、冬虫夏草组用6%冬虫夏草浸出液(10 mL/kg)加硫唑嘌呤1.0 mg/(kg·d)灌胃.于治疗21 d后,测定肝微粒体细胞色素P450亚型酶(CYPIA2、CYP2C9、CYP2D6、CYP2E1、CYP3A4)活性,血清总蛋白、白蛋白、血红蛋白,静脉血红细胞、白细胞、T淋巴细胞、单核细胞数量,受体大鼠感染率.结果 冬虫夏草浸出液明显抑制存活受体大鼠P450亚型酶CYPIA2(0.68±0.09)、CYP3A4酶的活性(4.92±0.27),降低静脉血红细胞(6.71±0.87)、白细胞数量(10.36±0.09),提高血清总蛋白(19.39±4.93)、白蛋白(14.27±4.45)及血红蛋白含量(19.39±4.973),明显降低受体大鼠感染率40.87%.与硫唑嘌呤组比较,P<0.05.对T淋巴细胞及单核细胞数量无明显影响,与硫唑嘌呤组比较,P>0.05.结论 冬虫夏草浸出液在不影响硫唑嘌呤抑制肝移植排斥反应的同时,改善肝脏移植后低蛋白血症,提高体液免疫,对细胞免疫功能无明显影响,具有双向免疫调节作用. 相似文献
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目的:通过建立稳定的大鼠原位肝移植模型,总结实用性的手术技巧及常见并发症的防治措施。方法:采用改良的二袖套法施行大鼠原位肝移植术123次,观察并分析手术时间、存活率及手术并发症。结果:手术成功率93.5%(115/123),一周存活率为83.7%(103/123),手术并发症主要有麻醉意外、失血性休克、吻合口出血、胆道梗阻、胆漏等。结论:改进的手术方法可以提高手术的成功率,减少并发症的发生。 相似文献
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目的:研究前列地尔脂微球载体制剂对脑死亡状态下SD大鼠肝脏功能和形态的影响。方法:选取SD大鼠24只,随机分为4组,即脑死亡组(B组):应用改进的缓慢间断颅内加压法建立脑死亡模型;假手术组(C组):除不进行硬脑膜外导管加压外,其余处理同脑死亡组;前列地尔干预1,2组(L1,L2):建立脑死亡模型,L1,L2组分别于SD大鼠确认脑死亡后,持续泵入前列地尔脂微球载体制剂20,40 ng/(kg·min) 至实验结束。抽取血标本检测丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、肿瘤坏死因子-α(TNF-α)、内皮素-1(ET-1) 水平。于脑死亡后6 h取材,切取肝脏组织标本包埋固定,切片,HE染色观察肝细胞损伤情况。结果:在脑死亡时,B,L1和L2组ALT,AST,ET-1,TNF-α水平与C组比较,差异有统计学意义(P<0.05),L1和L2组低于B组,差异有统计学意义(P<0.05),L2组与L1组比较,差异无统计学意义(P>0.05)。结论:SD大鼠脑死亡状态下肝脏可发生损伤性改变。前列地尔脂微球载体制剂能减轻脑死亡状态下大鼠肝脏的损伤。 相似文献
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目的 研究自体肝片大网膜移植后,肝片生长情况,为肝脏外科临床及实验研究提供理论依据.方法 Wistar大鼠20只,随机分为4组,5只大鼠均左外肝叶切除自体肝片大网膜移植,分别于术后3、7、14、21d分批处死动物.肉眼观察移植物颜色、大小及粘连情况,HE法染色,常规光镜观察移植肝片在不同时期的组织学特点.结果 自体肝片移植术后3d 即有血管从移植肝片周围大网膜向肝片内伸展,伴肝细胞凝固性坏死,随时间推移肝片进一步坏死至消失.结论 自体肝片大网膜内移植是简便的肝移植方法,但其存活性有待进一步深入研究. 相似文献
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目的探讨脑死亡状态对巴马小型猪肝脏的影响及其机制。方法巴马小型猪15只,随机分脑死亡组(B组)、灯盏花素处理组(P组)和对照组(C组),每组5只。用颅内加压法建立脑死亡模型。建模成功后,B组不行其他处理;P组分别于初次确认脑死亡后1、12h时灯盏花素按2.5mg/kg,加入100ml生理盐水中,静脉滴注;C组仅开颅麻醉维持。脑死亡3、6、12、18和24h取血清测丙氨酸转移酶(ALT)、天冬氨酸转氨酶(AST)及肿瘤坏死因子α(TNFα)、IL1β、IL6水平。取脑死亡后6、12和24h点肝组织行HE染色并免疫组化法测蛋白激酶Cα(PKCα)的表达水平并RT PCR法测PKCαmRNA的变化,12、24h点肝组织观察肝脏超微结构变化。结果初次判定巴马小型猪脑死亡后12、18和24h:ALT水平C组分别为33.0±6.7、29.0±1.6和(36.6±5.6)U/L,B组分别为141.8±9.1、191.4±10.9和(238.6±10.4)U/L,P组分别为91.0±4.9、131.6±6.4和(175.6±7.0)U/L;AST水平C组分别为27.4±3.9、29.8±1.6和(29.2±3.4)U/L;B组分别为91.4±8.1、126.6±5.5和(184.4±5.4)U/L;组分别为59.2±6.1、86.8±5.5和(146.2±6.4)U/L;B组血清ALT、AST水平随着脑死亡时间的延长逐渐升高;明显高于C组,P组两者水平亦升高,但升高幅度较B组低。炎症介质在首次判定脑死亡后3、6、12、18和24h的IL1β水平,C组分别为5.91±0.17、5.91±0.10、6.06±0.12、6.08±0.12和(6.10±0.15)pg/ml,B组分别为8.26±0.21、9.17±0.08、10.30±0.11、12.53±0.35和(16.37±0.16)pg/ml,P组分别为7.75±0.12、8.08±0.11、9.25±0.21、11.44±0.19和(15.43±0.36)pg/ml;IL6水平C组分别为17.35±0.59、18.04±0.23、17.99±0.83、17.77±1.05和(17.62±0.67)pg/ml,B组分别为29.50±1.92、37.92±1.69、46.32±1.70、56.62±1.95和(66.68±2.11)pg/ml,P组分别为21.27±1.05、23.65±1.09、31.46±1.91、37.60±1.75和45.16±1.9pg/ml;TNFα水平,C组分别为14.94±0.36、15.03±0.49、14.71±0.46、14.66±0.31和(14.64±0.63)pg/ml,B组分别为19.45±0.16、21.76±0.25、24.31±0.20、27.65±0.27和(31.35±0.16)pg/ml,P组分别为18.45±0.11、20.21±0.41、23.41±0.32、26.17±0.21和(28.36±0.20)pg/ml;B组血清IL1β、IL6和TNFα水平随着脑死亡时间的延长逐渐升高;明显高于C组,P组三者水平亦升高,但升高幅度较B组低。6、12和24h的肝细胞中PKCα蛋白表达水平,C组分别为0.0887±0.0113、0.0950±0.0284和0.0994±0.0113,B组分别为0.1508±0.0108、0.3811±0.0382和0.6209±0.0312,P组分别为0.1091±0.0292、0.1284±0.0142和0.2995±0.0276;6、12和24h肝细胞中PKCαmRNA表达水平,C组分别为5782±594、5501±423和5729±533,B组分别为26789±3059、32877±5526和39869±6548,P组分别为24027±5012、20409±4793和14307±3786。PKCα蛋白在C组肝细胞表达在胞浆内,仅见少量阳性细胞,B组6h可见肝脏中阳性细胞显著增多,P组PKCα蛋白表达阳性细胞较B组低。3脑死亡后肝脏中PKCαmRNA的变化与PKCα蛋白变化趋势相同。肝脏光镜及电镜下肝脏损伤变化B组明显重于C组,P组在脑死亡后12h仅出现细胞水肿。结论脑死亡状态下肝脏出现功能与形态学的损伤性变化;PKCα可能参与了这种损伤机制,灯盏花素能够抑制动物肝脏中PKC-α的活化,灯盏花素处理可以减轻肝脏这种损伤。 相似文献
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目的:探讨人神经干细胞(NSCs)移植治疗大鼠脑创伤的可行性.方法:取孕14周流产胎儿脑组织,进行NSCs培养及鉴定,并应用Hoechest33258标记细胞.54只大鼠随机等分为假损伤组(A组)、治疗对照组(B组)及NSCs移植组(C组).采用自由落体撞击法制作大鼠脑创伤模型后,C组给予NSCs移植,B组给予生理盐水,A组不打击脑组织.3组分别于移植术后2 d及7 d进行大鼠行为学评分,分别于植术后2周和4周行Y迷宫试验测学习和记忆评分.移植后3 d、7 d脑组织切片荧光显微镜下观察移植细胞存活情况,移植后2周、4周行GFAP、NSE免疫组织化学染色.结果:NSCs移植后2 d行为学评分3组之间差异有统计学意义(P=0.00),B、C组间差异无统计学意义(P=0.09);移植后7 d行为学评分3组间差异有统计学意义(P=0.00),A、C组间差异无统计学意义(P=0.10);移植后2周学习评分和4周记忆评分3组间差异均有统计学意义(P=0.00),B、C组间差异均有统计学意义(P=0.00);C组脑组织GFAP、NSE染色阳性,可见标记的NSCs.结论:人NSCs植入大鼠创伤脑内后,可存活并和宿主组织融合在一起,促进大鼠行为学恢复,提高学习和记忆能力,并分化为神经元和神经胶质细胞.NSCs移植为治疗脑创伤提供了新的方法. 相似文献
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Ming Yingzi Shao Mingjie Tian Tingting She Xingguo Liu Hong Ye Shaojun Ye Qifa 《中华医学杂志(英文版)》2014,127(15):2829-2836
Background Our goal was to evaluate the outcomes of kidney transplants from controlled cardiac death donors compared with brain death donors by conducting a meta-analysis of cohort studies.Methods The PubMed database and EMBASE were searched from January 1980 to July 2013 to identify studies that met pre-stated inclusion criteria.Reference lists of retrieved articles were also reviewed.Two authors independently extracted information on the designs of the studies,the characteristics of the study participants,and outcome assessments.Results Nine cohort studies involving 84 398 participants were included in this meta-analysis; 3 014 received kidneys from controlled cardiac death donors and 80 684 from brain death donors.Warm ischemia time was significantly longer for the controlled cardiac death donor group.The incidence of delayed graft function was 2.74 times (P 〈0.001) greater in the controlled cardiac death donor group.The results are in favor of the brain death donor group on short-term patient and graft survival while this difference became nonsignificant at mid-term and long term.Sensitivity analysis yielded similar results.No evidence of publication bias was observed.Conclusion This meta-analysis of retrospective cohort studies suggests that the outcome after controlled cardiac death donors is comparable with that obtained using kidneys from brain death donors. 相似文献
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Carbon monoxide inhalation ameliorates conditions of lung grafts from rat brain death donors 总被引:3,自引:0,他引:3
Background Successful lung transplantation has been limited by the scarcity of donors. Brain death (BD) donors are major source of lung transplantation. Whereas BD process induces acute lung injury and aggravates lung ischemia reperfusion injury. Carbon monoxide (CO) inhalation at 50-500 parts per million (ppm) can ameliorate lung injury in several models. We examined in rats whether CO inhalation in BD donor would show favorable effects on lung grafts. Methods Rats were randomly divided into 4 groups. In sham group, donor rats received insertion of a balloon catheter into the cranial cavity, but the balloon was not inflated. In BD-only group, donor rats were ventilated with 40% oxygen after BD confirmation. In BD+CO250 and BD+CO500 groups, donor rats inhaled, after BD confirmation, 250 ppm or 500 ppm CO for 120 minutes prior to lung procurement, and orthotopic lung transplantation was performed. The rats were sacrificed 120 minutes after the lung transplantation by exsanguination, and their blood and lung graft samples were obtained. A total of 8 rats fulfilling the criteria were included in each group. Results The inhalation decreased the severity of lung injury in grafts from BD donors checked by histological examination. CO pretreatment reversed the aggravation of PaO2/FiO2 in recipients from BD donors. The CO inhalation down-regulated pro-inflammatory cytokines (TNF-α, IL-6) along with the increase of anti-inflammatory cytokine (IL-10) in recipient serum, and inhibited the activity of myeloperoxidase in grafts tissue. The inhalation significantly decreased cell apoptosis in lung grafts, inhibiting mRNA and protein expression of intercellular adhesion molecule-1 (ICAM-1) and caspase-3 in lung grafts. Further, the inhalation activated phosphorylation of p38 expression and inhibited phosphorylation of anti-extracellular signal-regulated kinase (ERK) expression in lung grafts. The effects of CO at 500 ppm were greater than those at 250 ppm. Conclusions CO exerts potent protective 相似文献
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目的:探索创伤性脑损伤病理过程中p53诱导死亡结构域蛋白(PIDD)的表达变化。方法:建立大鼠脑损伤模型,采用免疫印迹法和免疫组织化学法检测损伤后的大鼠皮层组织中PIDD的表达和定位变化。结果:(1)在假手术脑组织中,PIDD表达很低,脑损伤后其表达逐渐增加,在3天左右达到最高峰,之后表达下降;(2)免疫组织化学法和免疫荧光实验表明,PIDD在损伤后的脑组织中表达明显上升,并且主要定位于神经元之中。 相似文献
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肾移植术后早期环孢菌素A引起的肝损害 总被引:1,自引:1,他引:0
目的探讨肾移植术后3个月CsA免疫抑制剂的肝损害治疗措施.方法对19例出现肝功能异常的病例进行分析,测定肝功能异常时CsA的谷值浓度.及时调节免疫抑制剂用量,配合保肝利胆治疗.结果17例于2~4周肝功能恢复正常.2例无效,将CsA改为FK506后1个月后,肝功能指标逐渐恢复正常.结论低剂量CsA、MMF、pred三联是目前理想的免疫抑制治疗方案,结合保肝治疗,对减少术后早期CsA肝毒性的发生有一定疗效. 相似文献
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目的 初步研究A20在小移植物损伤中的地位和作用,为临床应用提供理论依据。方法 选取雄性SD大鼠,分为正常对照组、全肝移植组和小体积肝移植组3组,在移植后0.5及3、6、24h的4个时间点分别取材、送检。主要进行肝功能检测及肝组织病理组织学检查;采用原位末端标记法(TUNEL法)检测细胞凋亡情况,逆转录聚合酶链反应(RT-PCR)检测A20在肝组织中的表达,Westernblot检测肝组织内蛋白的表达。结果 移植后各时点丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)水平均升高,至术后6h达到高峰,组织病理学检查可见小体积肝移植组移植后6h损伤最重。TUNEL法细胞凋亡检查见小体积肝移植组各时间点细胞凋亡数均显著多于全肝移植组,移植后6h为高峰。Western blot和RT-PCR法在不同水平检测结果提示保护性基因A20在小体积肝移植组的移植物内表达下降,并随再灌注时间的延长迅速下调。结论 大鼠小体积肝移植术后再灌注损伤以肝细胞功能改变及大量肝细胞凋亡为特点。肝组织内保护性基因A20的下调可能是小移植物缺血再灌注损伤发生的重要始动环节之一。 相似文献
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目的 探讨肝移植后再灌注损伤和排斥反应时,肝窦内皮细胞的变化。方法 利用抗肝窦内皮细胞的单克隆抗体对大鼠肝移植后定期采取的肝组织标本染色。结果 对照组(LEW-LEW)于第4天在肝窦壁内可见ICAM-1的强染色,但是昆布氨酸、第Ⅷ因子相关抗原在实验基间均未见到。高度排斥反应组(ACI-LEW)移植后第1在开始发现ICAM-1的强染色。中度排斥反应组(BN-LEW)移植后第1天开始发现ICAM-1的强染色,移植后1个月开始肝窦壁出现第Ⅷ因子相关抗原。结论 说明慢性排斥反应引起的肝损伤,不仅是以肝动脉为中心的血管损伤,同时也损伤肝窦内皮细胞。 相似文献
18.
Multiple procedures of liver transplantation bring conditions producing cold ischemia-reperfusion (I/R) injury. During cold storage, the graft organ is subjected to cold ischemia, also known as hypoxia injury. After reperfusion, although hypoxic condition has been ameliorated, reoxygenation of the graft liver can produce not only reperfusion injury including generation of oxygen free radical, lipoperoxidation and calcium overload, but also aggravate the hypoxia damage, 相似文献
19.
Donation after brain death followed by circulatory death (DBCD) is a unique practice in China. The aim of this study was to define the pathologic characteristics of DBCD liver allografts in a porcine model. Fifteen male pigs (25-30 kg) were allocated randomly into donation after brain death (DBD), donation after circulatory death (DCD) and DBCD groups. Brain death was induced by aug- menting intracranial pressure. Circulatory death was induced by withdrawal of life support in DBCD group and by venous injection of 40 mL 10% potassium chloride in DCD group. The donor livers were perfused in situ and kept in cold storage for 4 h. Liver tissue and common bile duct samples were col- lected for hematoxylin and eosin staining, TUNEL testing and electron microscopic examination. Spot necrosis was found in hepatic parenchyma of DBD and DBCD groups, while a large area of necrosis was shown in DCD group. The apoptosis rate of hepatocytes in DBD [(0.56±0.30)%] and DBCD [(0.50 ±0.11)%] groups was much lower than that in DCD group [(3.78±0.33)%] (P〈0.05). And there was no significant difference between DBD group and DBCD group (P〉0.05)). The structures of bile duct were intact in both DBD and DBCD groups, while the biliary epithelium was totally damaged in DCD group. Under electron microscope, the DBD hepatocytes were characterized by intact cell membrane, well-organized endoplasmic reticulum, mild mitochondria edema and abundant glycogens. Broken cell membrane, mild inflammatory cell infiltration and sinusoidal epithelium edema, as well as reduced glycogen volume, were found in the DBCD hepatocytes. The DCD hepatocytes had more profound cell organelle injury and much less glycogen storage. In conclusion, the preservation injury of DBCD liver allografts is much less severe than that of un-controlled DCD, but more severe than that of DBD liver allografts under electron microscope, which might reflect post-transplant liver function to some extent. 相似文献
20.
目的:观察大鼠创伤性脑损伤后Numbl的表达变化及其与脑损伤的关系。方法:构建大鼠创伤性脑损伤模型,收集蛋白并做冰冻切片,采用Western Blot及免疫组化分析Numbl的表达变化及分布,免疫荧光双标分析Numbl的细胞定位。结果:大鼠创伤性脑损伤后Numbl的表达降低,其主要分布在损伤区域的皮质中,免疫荧光显示Numbl主要定位于皮质的神经元中。结论:Numbl在大鼠创伤性脑损伤后表达减少,其主要定位于损伤区域的神经元中,有可能参与损伤诱导的神经元的凋亡及再生。 相似文献