Establishment of an animal model of ischemic type intrahepatic biliary lesion in rabbits

AIM:To explore a method to establish an animal model of ischemic type intrahepatic biliary lesion in rabbits. METHODS:Forty Japanese white rabbits of clean grade were divided randomly into four groups(10 rabbits per group)including sham operation(SO) group,and artery-bile obstruction(ABO)-1 h group, ABO-2 h group and ABO-3 h group.All the rabbits in this study underwent the same initial surgical procedure in which the liver was prepared as for graft removal during liver transplantation.Subsequently in the SO group,no additional vascular intervention was performed,while in groups ABO-1 h,ABO-2 h and ABO-3 h,the animals underwent combined clamping of the hepatic artery and common bile duct with microvascular clips for 1,2 and 3 h,respectively.After the scheduled occlusion time,the clip was removed to recover blood supply.The animals were killed 4 wk after operation.The survival rate,liver function, cholangiography and histopathological manifestation of the rabbits in each group were observed. RESULTS:The survival rate was 100%in groups SO,ABO-1 h and ABO-2 h,while it was 60%in group ABO-3 h.At each observation time,the change degree of the indexes of liver function was proportional to the clamping time(ABO-3 h>ABO-2 h>ABO-1 h> SO,P<0.05).Cholangiographical and histopathologic manifestations both showed that intrahepatic biliary lesion aggravated proportionally with the increase of the clamping time. CONCLUSION:An animal model of ischemic type intrahepatic biliary lesion in rabbits is successfully established,which may provide a reliable technique for basic and clinical research into the etiology, development and prophylaxis of ischemic type intrahepatic biliary lesion after liver transplantation.

Changes and significances of SOD and MDA after ischemia reperfusion injury of hepatic neoplasm

To explore the influence and significance of the ischemia reperfusion on the hepatic neoplasm, the hepatic VX2 neoplasm model of rabbits was established under the guide of ultrasonography; and ischemia was caused by using a non-traumatic vascular clamp to block the branches distributing in the left-middle lobe of the hepatic artery for 60 min, and subsequently the clamp was removed and the reperfusion injury of hepatic neoplasm occurred. At different time-points, the normal and hepatic neoplasm tissues of the animal models were taken out to detect the superoxide dismutase (SOD) and malondialdehyde (MDA) respectively.The results show that the products and injurious effects of oxygen free radical (OFR) of the neoplasm tissues are more serious than those of the normal hepatic tissues.

Intravenous administration of glutathione protects parenchymal and non-parenchymal liver cells against reperfusion injury following rat liver transplantation

AIM:To investigate the effects of intravenous administration of the antioxidant glutathione (GSH) on reperfusion injury following liver transplantation. METHODS:Livers of male Lewis rats were transplanted after 24 h of hypothermic preservation in University of Wisconsin solution in a syngeneic setting.During a 2-h reperfusion period either saline (controls,n=8) or GSH (50 or 100 μmol/(h·kg),n=5 each) was continuously administered via the jugular vein. RESULTS:Two hours after starting reperfusion plasma ALT increased to 1 457±281 U/L (mean±SE) in controls but to only 908±187 U/L (P<0.05) in animals treated with 100 μmol GSH/(h·kg).No protection was conveyed by 50μmol GSH/(h·kg).Cytoprotection was confirmed by morphological findings on electron microscopy:GSH treatment prevented detachment of sinusoidal endothelial cells (SECs) as well as loss of microvilli and mitochondrial swelling of hepatocytes.Accordingly,postischemic bile flow increased 2-fold.Intravital fluorescence microscopy revealed a nearly complete restoration of sinusoidal blood flow and a significant reduction of leukocyte adherence to sinusoids and postsinusoidal venules.Following infusion of 50μmol and 100 μmol GSH/(h·kg),plasma GSH increased to 65±7 mol/L and 97±18 mol/L,but to only 20±3 mol/L in untreated recipients. Furthermore,plasma glutathione disulfide (GSSG) increased to 7.5±1.0 mol/L in animals treated with 100μmol/(h·kg) GSH but infusion of 50μmol GSH/(h·kg) did not raise levels of untreated controls (1.8±0.5 mol/L vs 2.2±0.2 mol/L). CONCLUSION:Plasma GSH levels above a critical level may act as a “sink” for ROS produced in the hepatic vasculature during reperfusion of liver grafts.Therefore,GSH can be considered a candidate antioxidant for the Drevention of reperfusion injury after liver transplantation,in particular since it has a low toxicity in humans.

Hydrogen sulfide intervention in focal cerebral ischemia/reperfusion injury in rats

The present study aimed to explore the mechanism underlying the protective effects of hydrogen sulfide against neuronal damage caused by cerebral ischemia/reperfusion. We established the middle cerebral artery occlusion model in rats via the suture method. Ten minutes after middle cerebral artery occlusion, the animals were intraperitoneally injected with hydrogen sulfide donor compound sodium hydrosulfide. Immunofluorescence revealed that the immunoreactivity of P2X7 in the cerebral cortex and hippocampal CA1 region in rats with cerebral ischemia/reperfusion injury decreased with hydrogen sulfide treatment. Furthermore, treatment of these rats with hydrogen sulfide significantly lowered mortality, the Longa neurological deficit scores, and infarct volume. These results indicate that hydrogen sulfide may be protective in rats with local cerebral ischemia/reperfusion injury by down-regulating the expression of P2X7 receptors.

Japanese herbal medicine, Saiko-keishi-to, prevents gut ischemia/reperfusion-induced liver injury in rats via nitric oxide

AIM:To determine whether Saiko-keishi-to(TJ-10),a Japanese herbal medicine,could protect liver injury induced by gut ischemia/reperfusion(I/R),and to investigate the role of NO. METHODS:Male Wistar rats were exposed to 30-min gut isohemia followed by 60 min of reperfusion.Intravital microscopy was used to monitor leukocyte recruitment.Plasma tumor necrosis factor(TNF)levels and alanine aminotransferase (ALT)activities were measured.TJ-10 1 g/(kg.d)was intragastrically administered to rats for 7 d.A NO synthase inhibitor was administered. RESULTS:In control rats,gut I/R elicited increases in the number of stationary leukocytes,and plasma TNF levels and ALT activities were mitigated by pretreatment with TJ-10.Pretreatment with the NO synthase inhibitor diminished the protective effects of TJ-10 on leukostasis in the liver,and the increase of plasma TNF levels and ALT activities.Pretreatment with TJ-10 increased plasma nitrite/nitrate levels. CONCLUSION:TJ-10 attenuates the gut I/R-induced hepatic microvascular dysfunction and sequential hepatocellular injury via enhancement of NO production.

Biliary tract injury caused by different relative warm ischemia time in liver transplantation in rats

BACKGROUND: There is a controversy over the degree of liver and biliary injury caused by the period of secondary warm ischemia. A liver autotransplantation model was adopted because it excludes the effects of infection and immunological rejection on bile duct injury. This study was undertaken to assess biliary tract injury caused by relative warm ischemia (secondary warm ischemia time in the biliary tract) and reperfusion. METHODS: One hundred and two rats were randomly divided into 5 groups: group I (control); groups 11 to V, relative warm ischemia times of 0 minute, 30 minutes, I hour and 2 hours. In addition to the levels of serum alkaline phosphatase, and total bilirubin, pathomorphology assessment and TUNEL assay were performed to evaluate biliary tract damage. RESULTS: Under the conditions that there were no significant differences in warm ischemia time, cold perfusion time and anhepatic phase, group comparisons showed statistically significant differences. The least injury occurred in group H (portal vein and hepatic artery reperfused simultaneously) but the most severe injury occurred in group V (biliary tract relative warm ischemia time 2 hours). CONCLUSIONS: Relative warm ischemia is one of the factors that result in bile duct injury, and the relationship between relative warm ischemia time the bile injury degree is time-dependent. Simultaneous arterial and portal reperfusion is the best choice to avoid the bile duct injury caused by relative warm ischemia. (Hepatobiliary Pancreat Dis Int 2009; 8: 247-254)

长链非编码RNA-N1LR在脑缺血再灌注血脑屏障损伤的作用机制研究

目的探讨长链非编码RNA(lncRNA)-N1LR在脑缺血再灌注损伤后血脑屏障的作用机制。方法原代小鼠脑微血管内皮细胞常规培养,经氧糖剥夺/复糖复氧(OGD/R)处理模拟脑缺血再灌注损伤,实验分对照组、OGD组、lncRNA-N1LR过表达组(OGD处理后转染质粒lncRNA-N1LR过表达)、lncRNA-N1LR沉默组(OGD处理后转染质粒lncRNA-N1LR沉默)。采用逆转录聚合酶链反应检测各组中lncRNA-N1LR mRNA、紧密连接蛋白5(claudin-5)及闭合蛋白(occludin)mRNA表达水平;异硫氰酸荧光素-葡聚糖(FITC-dextran)渗透法检测血脑屏障通透性;免疫蛋白印迹法检测claudin-5、occludin蛋白表达。结果与对照组比较,OGD组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平下降(0.31±0.01 vs 1.00±0.10,0.42±0.03 vs 1.01±0.13,0.38±0.03 vs 1.00±0.15,P<0.05),血脑屏障FITC-dextran通透性明显升高(58.79±3.04 vs 8.87±0.63,P<0.01)。与OGD组比较,lncRNA-N1LR过表达组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平升高(0.67±0.07 vs 0.31±0.01,0.92±0.02 vs 0.42±0.03,0.70±0.08 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性降低(41.57±2.43 vs 58.79±3.04,P<0.05)。与OGD组比较,lncRNA-N1LR沉默组lncRNA-N1LR mRNA、occludin、claudin-5 mRNA表达水平降低(0.21±0.02 vs 0.31±0.01,0.31±0.03 vs 0.42±0.03,0.22±0.02 vs 0.38±0.03,P<0.05),血脑屏障FITC-dextran通透性升高(72.34±1.43 vs 58.79±3.04,P<0.05)。结论LncRNA-N1LR上调可能通过降低血脑屏障通透性发挥神经保护作用。

银杏内酯B对脂肪肝小鼠肝脏缺血再灌注损伤的影响及其机制

目的探究银杏内酯B对脂肪肝小鼠肝脏缺血再灌注损伤的影响及其机制。方法选择60%高脂饲料喂养16周的C57BL/6J雄性小鼠共25只,分为假手术组(开腹后缝合)、模型组(阻断肝中、左叶血流1 h后再灌注6 h)、银杏内酯B组(25 mg/kg银杏内酯B腹腔注射2次后同模型组处理)、GW9662组(1 mg/kg GW9662腹腔注射2次后同模型组处理)、GW9662+银杏内酯B组(25 mg/kg银杏内酯B+1 mg/kg GW9662混合溶液腹腔注射2次后同模型组处理)。给药并行手术后6 h检测各组小鼠血清谷丙转氨酶(ALT)、谷草转氨酶(AST)水平,免疫印迹法检测各组小鼠肝组织Bax、Bcl-2、PPARγ蛋白表达水平,油红O染色检测各组小鼠肝脏组织脂肪化程度,HE染色检测各组小鼠肝脏组织坏死程度。结果油红O染色结果显示,各组小鼠肝脏脂肪化程度已达脂肪肝水平。血清酶学检测结果显示,银杏内酯B组、GW9662+银杏内酯B组小鼠血清ALT、AST水平均显著低于模型组(P<0.05),银杏内酯B组小鼠血清ALT水平显著低于GW9662+银杏内酯B组(P<0.05)。HE染色结果显示,银杏内酯B组小鼠肝组织坏死面积百分比显著低于模型组及GW9662+银杏内酯B组(P<0.05)。免疫印迹结果显示,银杏内酯B组小鼠肝组织Bax表达水平显著低于模型组(P<0.05),而Bcl-2、PPARγ表达水平显著高于模型组及GW9662+银杏内酯B组(P<0.05)。结论银杏内酯B可通过上调肝组织PPARγ水平以减轻脂肪肝小鼠缺血再灌注损伤。

儿童体外循环手术压力性损伤发生风险因素及预测模型构建

目的通过对儿童体外循环手术压力性损伤的现状进行调查,构建一个预测模型,以便更好地理解和预测发生压力性损伤的风险。方法回顾性分析2021年7月至2023年12月湖南省儿童医院收治的儿童体外循环手术压力性损伤的相关数据,进行现状调查并构建预测模型。结果最终本研究共纳入研究对象283例,其中59例发生了压力性损伤,发生率为20.8%。性别、术前Braden评分、麻醉分级以及术中出血为儿童体外循环手术压力性损伤发生的影响因素(P<0.05)。预测模型:Logit(P)=-1.383+1.403×性别+1.149×麻醉分级-1.537×术前Braden评分+0.770×术中出血量,其灵敏度为0.749,特异度为0.832。结论儿童体外循环手术压力性损伤发生率较高,且受性别、术前Braden评分、麻醉分级以及术中出血量4个因素影响。基于以上4个危险因素构建的风险预测模型效果良好,可以为临床筛选儿童体外循环手术压力性损伤高危患儿。

体外循环中心肌缺血再灌注损伤与恢复的超微结构研究

目的：观察体外循环（ＣＰＢ）中心肌缺血及再灌注对心肌超微结构的影响，并评价持续冷血及温血停搏液灌注对心肌的保护作用。方法：采用猫ＣＰＢ模型，随机分成单纯ＣＰＢ（组Ⅰ）、单纯缺血再灌注（组Ⅱ）、持续冷血停搏液灌注（组Ⅲ）及持续温血停搏液灌注（组Ⅳ）４组。观察各组不同时间点心肌超微结构变化，并对超微结构进行半定量分析。结果：组Ⅱ的心肌超微结构变化较心脏缺血期间进一步加重，线粒体基质电子密度明显降低；线粒体内可见到Ｊｅｎｎｉｎｇ小体；毛细血管内皮细胞高度肿胀且不规则、基底膜断裂、血管腔明显狭窄；组Ⅲ和组Ⅳ则均为轻度至中度的变化，其中以组Ⅳ变化最轻，线粒体内未见Ｊｅｎ－ｎｉｎｇ小体形成；糖原颗粒大部分保存较好；升主动脉开放后１２０ｍｉｎ，组Ⅲ及组Ⅳ的心肌超微结构均有不同程度的恢复，其中以组Ⅳ最为明显。结论：ＣＰＢ中心肌的缺血再灌注损伤在心肌再灌注的３０ｍｉｎ最为明显，而且以线粒体及毛细血管内皮细胞的改变较为突出；持续冷血和温血停搏液灌注，对心肌均有一定程度的保护作用；持续温血停搏液灌注对心肌的超微结构的保护作用优于持续冷血停搏液灌注。

褥疮不完全性缺血再灌注损伤简易模型的建立

目的:建立一种简易的褥疮不完全性缺血再灌注损伤动物模型。方法:24只雄性SD大鼠随机分为3组:对照组(C组);不完全性缺血组(I组);不完全性缺血再灌注组(IR组)。通过肉眼观察大鼠受压部位皮肤形态和颜色,光镜下观察皮肤和肌肉组织的病理学变化,并测定大鼠血浆超氧化物歧化酶(SOD)、乳酸脱氢酶(LDH)活性和丙二醛(MDA)、内皮素-1(ET-1)、一氧化氮(NO)含量的变化。结果:I组和IR组皮肤肉眼观察均出现紫红色;皮肤和肌肉光镜下观察均出现损伤,其中IR组比I组更明显;I组与C组比较,其SOD活性以及MDA、ET-1、NO含量差异无显著差异(P>0.05),而LDH活性增加(P<0.05);IR组与C组、I组比较,其SOD活性、NO含量明显下降(P<0.05或P<0.01),LDH活性和MDA、ET-1含量明显升高(P<0.05或P<0.01)。结论:该模型以临床实际情况为基础,操作简便易行,可用于皮肤褥疮的机制和防治研究。

大鼠心肌缺血再灌注损伤模型的改进

目的 改进心肌缺血再灌注模型制备 ,提高制模成功率。方法 采用成年SD大鼠制作心肌缺血再灌注模型 ,对传统造模方法进行了改进 ,不做气管插管 ,不剪断肋骨 ,冠状动脉结扎在胸外进行 ,冠状动脉结扎前放一引线 ,避免了二次开胸。大大减少了造模时间 ,提高了造模成功率。用心电图J点抬高与高耸T融合呈弓背向上的单相曲线 ,肉眼观及病理检查作为判断结扎成功指标。结果 造模 2 5只 ,成功2 0只 ,成功率 80 %。结论 本方法造模成功率高 ,心脏暴露好、结扎可靠 ,操作简单、方便。

丙泊酚后处理对体外循环冠脉旁路移植术患者心肌缺血再灌注损伤的影响

目的:探讨主动脉开放即刻靶控输注丙泊酚1mg/L对体外循环下行冠状动脉旁路移植术患者心肌缺血再灌注损伤的影响。方法:择期体外循环下行冠状动脉旁路移植术患者40例,ASAⅡ级或Ⅲ级,随机分为七氟烷组(S组)和丙泊酚后处理组(P组)各20例。S组全程吸入0.5%～2%七氟烷;P组在主动脉开放前持续吸入0.5%～2%七氟烷,主动脉开放即刻靶控输注丙泊酚,血浆靶浓度为1mg/L,同时下调七氟烷吸入浓度,维持脑电双频谱指数(BIS)值在40～60范围直至手术结束。于麻醉诱导前即刻(T0)、主动脉开放后10min(T1)、回重症监护病房(ICU)后即刻(T2)、6h(T3)、12h(T4)、24h(T5)取桡动脉血测定心肌肌钙蛋白(IcTnI)、肌酸激酶同工酶(CK-MB)、可溶性细胞间黏附分子-1(sICAM-1)和CD11b水平。结果:2组不同时点cTnI、CK-MB、sICAM-1和CD11b浓度差异具有统计学意义(P<0.05);与S组比较,P组cTnI和CK-MB浓度在T3～5时降低、sICAM-1浓度在T2～5时降低、CD11b表达在T1～5时降低;2组术后心肌梗死、房颤和心肌缺血的发生率差异无统计学意义(P>0.05)。结论:体外循环下行冠状动脉旁路移植术患者于主动脉开放即刻靶控输注丙泊酚1mg/L可减轻心肌缺血再灌注损伤,具有后处理保护作用。

门静脉转流下入肝血流阻断动物模型的建立及评价

目的：设计一种可避免门静脉淤血的动物模型，排除门静脉淤血对肝脏功能恢复的影响，从而为肝脏耐受缺血时限的实验研究提供理想的实验模型。方法：利用大鼠肝脏解剖特点，分别阻断肝左、中、右叶肝蒂（ 约占全肝９５ ％ ） ，造成受累肝叶完全缺血；保留尾叶血供作为肝蒂阻断期间门静脉血经肝脏回流入下腔的通道，到预定观察终点，去除肝蒂阻断夹即恢复肝脏血流，切除尾状叶。经血管造影及染料示踪法观察肝蒂阻断后门静脉流出道的完整性及肝脏缺血的完全性以及肝蒂阻断前后血液动力学变化；并观察了肝脏再灌流后２４ ｈ 的病理变化及动物７ ｄ 存活率，与单纯入肝血流阻断组做对照。结果：这种新设计的门静脉转流下入肝血流阻断动物模型，肝脏缺血可靠，门静脉流出道完整，阻断肝蒂前后血液动力学稳定；肝脏病理变化及动物术后７ ｄ 存活率转流组与单纯入肝血流阻断组有明显差异，前者好于后者。结论：该模型复制方法简单、重复性高、对机体附加创伤和生理干扰小，是研究大鼠对入肝血流阻断耐受时限的理想模型。

持续灌注温血心脏停搏液对心肌保护作用的实验研究

用猫体外循环模型对比观察间断冷血、持续冷血及持续温血心脏停搏液灌注对心肌的保护作用。结果发现，心脏停搏３ｈ后心肌线粒体呼吸功能和氢化磷酸化能力，间断冷血组明显下降，持续冷血组呈轻度下降，持续温血组保持正常；而再灌注后间断冷血组和持续冷血组进一步下降，持续温血组仍保持正常。丙二醛含量间断冷血组明显增加，持续冷血组有增加趋势，再灌注后两组都进一步升高；而持续温血组始终维持在接近正常水平。表明持续灌注温血停搏液技术可使心脏在停搏期间有充足的血供，心肌不存在缺血、缺氧状态，消除了氧自由基产生的必要条件，有利于保护线粒体功能，同时避免了因缺血、缺氧所诱发的心肌再灌注损伤，是一种理想的心肌保护方法。

犬肠缺血/再灌注时小肠对早期肠内营养耐受能力的实验研究

目的研究肠道低灌注状态下实施早期肠内营养(EEN)时小肠功能指标及耐受能力的变化。方法健康雄性杂种犬24只,夹闭肠系膜上动脉(SM A)1 h后恢复灌注造成肠缺血/再灌注(I/R)损伤,复流后4 h实施EEN,将瑞代营养液(4 m l.k-g 1.-h 1)经肠黏膜张力计管持续滴注3 h,如果动物出现肠道不能耐受症状(如呕吐、腹泻等)则停止,间隔6 h后再次实施EEN,直至动物肠道能够耐受为止。按随机数字表法将动物分成单纯EEN组、单纯I/R组、I/R后EEN组(I/R+EEN组),每组8只。检测小肠黏膜二氧化碳分压(P iCO2)、D木糖吸收量、小肠腔内压力判定小肠灌注和功能变化。结果肠I/R+EEN组肠道不能耐受发生率(87.5%)和严重程度均显著高于单纯EEN组(0)和单纯I/R组(12.5%)。实施EEN后,与单纯I/R组和单纯EEN组相比,I/R+EEN组小肠腔内压力及肠P iCO2均显著升高,而血浆D木糖吸收量显著降低(P均<0.01)。结论肠I/R能显著降低小肠对EEN的耐受能力,肠I/R后过早(<12 h)实施EEN能加重小肠I/R损伤,并进一步抑制小肠吸收和运动功能。

高氧液对缺血再灌注家兔多脏器细胞损伤的保护作用

目的观察高氧液向人体组织细胞直接供氧,改善肌体的缺血缺氧状态,探讨高氧液对缺血再灌注家兔多脏器细胞损伤的保护作用。方法家兔36只,采用失血性休克模型,随机分为3组,检测多脏器组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、肿瘤坏死因子(TNF)含量及血浆酸性磷酸酶(ACP)、镁离子(Mg2+)浓度等,小肠组织作电镜观察。结果再灌注90min后,高氧液治疗组肝、肾、肺、肠等组织器官中的MDA和TNF水平低于对照组,SOD水平则高于对照组,血ACP、Mg2+浓度高氧液治疗组低于对照组;电镜观察,肠黏膜上皮细胞损伤,高氧液组不明显。结论高氧液对家兔缺血再灌注多脏器细胞的损伤有保护作用。

高压氧对大鼠脑缺血区线粒体氧自由基影响的实验研究

目的:研究高压氧(HBO)对大鼠脑缺血区线粒体氧自由基及抗自由基酶的影响。方法:参照改良的Koizumi方法,在激光多普勒血流仪监测局部脑血流的条件下,建立线栓法大鼠局灶性脑缺血模型,缺血90min后再灌注,缺血后3h高压氧治疗(3个标准大气压,1h),缺血后24h分别取缺血核心区和半暗区脑组织,差速离心提取线粒体,进行超氧阴离子自由基(O2.)生成速率、H2O2含量、丙二醛(MDA)含量测定,以及线粒体超氧化歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和还原型谷胱甘肽(GSH)含量测定。结果:脑缺血再灌注24h后缺血半暗区和核心区线粒体的H2O2、O2.、MDA的含量较正常对照组明显增加,而SOD、GSH-PX活性以及GSH的含量较正常对照组明显下降(P<0.05)。经HBO治疗后,缺血半暗区线粒体O2.含量增加(P<0.05),SOD活性提高(P<0.05),而MDA含量减少(P<0.05);缺血核心区线粒体O2.含量增加(P<0.05),SOD活性提高(P<0.05),但MDA含量不变。HBO治疗对脑缺血区的H2O2、GSH-PX和GSH作用无影响。结论:在脑缺血时间窗内,HBO治疗能增加脑缺血区线粒体自由基生成,提高线粒体抗自由基酶活性;能抑制脑缺血半暗区线粒体的脂质过氧化损伤,但对核心区作用不明显。提示线粒体的功能状态在HBO治疗后的自由基反应中起重要作用。

小鼠肺缺血再灌注损伤模型的建立与评估

目的探索一种用显微外科技术制备小鼠肺缺血再灌注损伤模型的方法,并对其效果进行评估。方法将30只C57BL/6J小鼠随机分成2组(缺血再灌注组和假手术组),每组15只。缺血再灌注组采用无创血管夹夹闭左肺门60min,再灌注120min,建立肺缺血再灌注模型。获取标本,检测肺湿干重比值,用光镜和电镜观察肺组织结构变化。结果肺缺血再灌注组湿干重比值明显高于假手术组(P<0.01),光镜、电镜下均可观察到严重的肺损伤改变。结论成功建立了小鼠肺缺血再灌注损伤模型,且方法简单,易于操作,成功率高,为肺缺血再灌注损伤机制研究提供了一种可行的模型。

线栓法大鼠缺血/再灌注脑损伤模型的改良

目的研究一种线栓法大鼠缺血/再灌注脑损伤模型的改良术式。方法结扎颈总动脉(CCA),不结扎颈外动脉和翼腭动脉,用头皮针于CCA结扎的远端穿刺导入3-0线栓造成缺血,通过拔出线栓形成再灌注。结果栓线长度(20.0±1.8)mm,造模成功率近70%,造模动物临床表现及病理表现典型。结论本术式简便,术者不需具备显微手术操作技巧,造模成功率较高。