乌司他丁联合缺血预处理对大鼠肝缺血再灌注损伤的影响

目的探讨乌司他丁(UTI)预处理和缺血预处理(IPC)联合应用对大鼠肝缺血再灌注损伤的影响及可能的作用机制。方法选择雄性SD大鼠50只,随机分为5组,分别为对照(sham)组、缺血再灌注(IR)组、IPC组、UTI组、UTI联合缺血预处理(UCI)组。术后采集下腔静脉血并取肝组织标本,检测血清AST、ALT、TNFɑ,肝组织髓过氧化物酶(MPO)、NF-κB、肝组织湿干比(W/D)及光镜观察肝组织病理形态学变化。计量资料组间比较采用单因素方差分析,进一步两两比较采用LSD-t检验。结果所检测的血清ALT、AST、TNFα水平和肝组织MPO、NF-κB、W/D值,IR组、IPC组、UTI组、UCI组均明显高于sham组(P值均<0.05),而IPC组、UTI组、UCI组均明显低于IR组(P值均<0.05),UTI组明显低于IPC组(P值均<0.05),UCI组明显低于IPC组、UTI组(P值均<0.05)。肝脏病理学检查示IR组、IPC组、UTI组、UCI组与sham组比较,肝组织损伤明显(P值均<0.05),而IPC组、UTI组、UCI组均比IR组肝组织损伤程度轻(P值均<0.05),UTI组肝组织损伤轻于IPC组(P值均<0.05),UCI组肝组织损伤轻于IPC组、UTI组(P值均<0.05)。结论 UTI和UCI对肝脏缺血再灌注损伤均有保护作用,二者联合应用时,明显增强了对肝脏缺血再灌注损伤的保护效应。其发生机制可能与抑制了NF-κB表达,减少TNFɑ、MPO的释放,减轻了肝脏的炎症反应有关。     

缺血预处理对脑缺血再灌注大鼠脑组织胶质纤维酸性蛋白表达的影响

目的 观察脑缺血预处理对脑缺血再灌注大鼠脑组织胶质纤维酸性蛋白(glial fibrillary acidic protein,GFAP)表达的影响,探讨星形胶质细胞活化在脑缺血耐受中的意义.方法 36只健康雄性Sprague-Dawley大鼠随机分为缺血预处理再缺血组、缺血组和对照组,每组12只,前2组分别在2 h大脑中动脉闭塞(middle cerebral artery occlusion,MCAO)前3 d给予10 min的MCAO预处理或假手术,第2次MCAO后24 h处死,对照组仅给予2次间隔3 d的假手术.比较各组脑梗死体积、组织病理学变化和GFAP表达.结果 缺血预处理后再缺血组和缺血组梗死体积分别为(136.85±14.51)mm3和(281.37±29.93)mm3,前者较后者显著缩小53.15%(P=0.007);同时,缺血预处理再缺血组神经元变性坏死显著减轻,并伴有GFAP表达显著上调(2组免疫组化染色平均吸光度分别为102.66±8.39和86.28±6.19,P=0.009).结论 缺血预处理可诱导脑缺血耐受,促进GFAP表达,星形胶质细胞活化可能是脑缺血耐受产生的机制之一.     

缺血预处理对脑缺血再灌注大鼠脑组织胶质纤维酸性蛋白表达的影响

Objective To observe the effect of focal cerebral ischemic preconditioning on the expression of glial fibrillary acidic protein (GFAP) and to investigate the significance of astrocyte activation in cerebral ischemic tolerance.Methods Thirty-six healthy male SpragueDawley rats were randomly divided into reischenmic,ischemic and control groups (n = 12 in each group) after ischemic preconditioning.The former two groups received 10 minutes middle cerebral artery occlusion (MCAO) preconditioning or sham operation 3 days before the 2-hour MCAO.The rats were killed 24 hours after the second MCAO.The control group only receivedthe two sham operations with an interval of three days.The infarct volume,histopathological changes,and GFAP expression in each group were compared.Results The infarct volume after ischemic preconditioning in the reischenmic and ischemic groups was 136.85 ± 14.51 mm3and 281.37 ± 29.93 mm3 respectively.The former was significantly reduced 53.15%compared to the latter (P =0.007).At the same time,neuronal degeneration and necrosis was reduced significantly,and GFAP expression was upregulated significantly (the mean absorbance for immunohistochemical staining in both groups was 102.66 ± 8.39 and 86.28 ± 6.19respectively,P = 0.009) after ischemic preconditioning in the reischemic group.Conclusions Focal ischemic preconditioning may induce brain ischemic tolerance and promote GFAP expression.The activation of astrocytes may be one of the mechanisms of cerebral ischemic tolerance.     

盐酸曲美他嗪预处理对大鼠肾脏急性缺血再灌注损伤的影响

目的：观察盐酸曲美他嗪（ TMZ）预处理对大鼠肾组织急性缺血再灌注损伤（ IRI）的影响。方法选择SD大鼠90只,随机均分为A、B两组：A组给予TMZ 10 mg／kg灌胃5 d后,建立缺血再灌注（IR1）、缺血再灌注后处理（IPO1）、假手术（S1）模型;B组生理盐水灌胃5 d后,建立缺血再灌注（IR2）、缺血再灌注后处理（IPO2）、假手术（S2）模型。检测各组末次恢复肾脏血供0、6、12、24、48 h后血清SCr、BUN、NGAL、IL-18水平;HE染色光镜下观察缺血-再灌注石蜡包埋切片肾组织损伤形态学改变。结果 IR1组与IPO1组相比,在各时间点各指标均无显著性差异。 IR1组与IR2组相比,在6 h时IR2组的NGAL、IL-18、肾小管损伤程度评分上升,12 h时BUN亦上升,24 h时IR2组的各项指标均高于IR1组,48 h时BUN、SCr高于IR1组（P均＜0．05）。 IPO1组与IPO2组相比,在6 h时IPO两组的NGAL明显上升,12 h时除SCr外均上升,24 h时除NGAL外其他指标均高于IPO1组,48 h时BUN、SCr、肾小管损伤评分程度高于IPO1组（ P均＞0．05）。 IR1组与IPO2组相比,在6 h时IPO2组NGAL上升,12 h时除SCr外其他指标均高于IR1组,48 h时SCr仍显著高于IR1组（P均＞0．05）。结论在大鼠肾脏IRI发生之前即预防性使用TMZ可减轻其肾功能损伤。     

缺血预处理对大鼠脑缺血再灌注损伤保护作用的探讨

目的探讨缺血预处理对大鼠脑缺血再灌注损伤的保护作用及其机制。方法SD大鼠随机分为三组,分别为假手术组、脑缺血再灌注组、脑缺血预处理组。各组采用Longa等的大脑中动脉线栓法并加以改进,制备缺血预处理及缺血再灌注损伤实验动物模型。比较各组神经功能缺失评分、脑梗死体积、血清NSE含量及脑组织IL-1β和TNF-α含量。结果脑缺血预处理可使神经功能缺损减轻、脑梗死体积缩小、血清NSE含量降低,脑组织IL-1β和TNF-α含量降低。结论缺血预处理可诱导脑缺血耐受作用的产生,下调脑组织再灌注损伤时IL-1β和TNF-α的表达,对脑缺血再灌注损伤具有保护作用。     

预处理对肝脏再灌注损伤大鼠肝组织、血液中NO和ET的影响及意义

目的　探讨预处理对肝脏缺血再灌注损伤大鼠肝组织和血液中一氧化氮 (NO)和内皮素 (ET)含量的影响及意义。方法　建立肝脏 70 %缺血再灌注损伤大鼠模型 ,分为对照组、缺血组、缺血预处理组、L -精氨酸组(L - arg)、Nω-硝基 - N -精氨酸甲酯 (L - NAME)组 ,观察各组肝功能变化 ,检测肝组织和血清中 NO和 ET及透明质酸 (HA)水平。结果　预处理可减轻 NO水平的下降和血浆 ET的升高 ,防止肝功酶的升高 (P<0 .0 5 )。结论　预处理可诱导缺血再灌注损伤大鼠 NO产生增加、ET产生减少 ,进而改善其微循环 ,减少再灌注损伤。     

缺血预处理对老年大鼠肝硬化肝脏保护作用及其机制探讨

目的　探讨缺血预处理对老年大鼠肝硬化肝脏缺血再灌注损伤的保护作用和机制。　方法　老年肝硬化SD雄性大鼠 40只 ,随机分为 5组 ,每组 8只。以肝组织ATP、ADP、AMP、能荷及血清丙氨酸氨基转移酶 (ALT)、天冬氨酸氨基转移酶 (AST)、乳酸脱氢酶 (LDH)和肝脏胆汁分泌量来评价肝功能 ,检测肝组织P 选择素蛋白表达并计算肝组织中性粒细胞浸润数。　结果　缺血再灌注 12 0min后 ,缺血预处理 (IPC)组和精氨酸预处理 (APC)组ATP含量和能荷水平明显高于缺血再灌注 (I/R)组〔分别为 (4 1± 1 6)、(4 0± 1 6)、(1 5± 0 6)U/L和 (0 6± 0 1)、(0 6± 0 1)、(0 4± 0 1)U/L ,均为P<0 0 1〕 ,而Nω 硝基 L 精氨酸甲酯预处理 (NPC)组与I/R组间差异无显著性 (P >0 0 5 )。IPC组和APC组ALT、AST、LDH受到明显抑制 (P <0 0 1)。肝组织胆汁分泌量 ,IPC组明显多于I/R组〔(0 10±0 0 3 )和 (0 0 7± 0 0 3 )ml/g肝组织 ,P <0 0 1〕 ,APC组与I/R组差异有显著性 (P <0 0 1)。IPC组和APC组中白细胞浸润受到抑制。I/R组肝细胞P 选择素蛋白表达显著增强 (P <0 0 1) ,IPC组和APC组明显抑制 ,而NPC组增强 (P <0 0 1)。肝组织中P 选择素蛋白表达与中性粒细胞浸润数之间呈显著正相关 (r=0 60 ,P <0 0 1)。     

Protective effects of glutamine preconditioning on ischemia-reperfusion injury in rats

BACKGROUND:Hepatic ischemia-reperfusion injury is a common phenomenon in hepatic surgical procedures and can result in further severe damage.This study aimed to investigate the protective effects of glutamine preconditioning on hepatic ischemia-reperfusion injury in rats and its dose-dependency. METHODS:Thirty-two healthy male Wistar rats were randomly divided into four groups(n=8 per group).One group received 0.9%NaCl(control)and the other three received glutamine(Gln groups)4 hours before ischemia.The Gln...     

右美托咪定联合远隔缺血预处理对心肌缺血/再灌注损伤的影响

目的 研究右美托咪定联合远隔缺血预处理对心肌缺血/再灌注损伤（MI/RI）的影响以及探讨其对细胞凋亡的影响 方法 选取80例择期体外循环下行心脏瓣膜术病患，随机分成4组(n = 20)；对照组（C组）, 远隔缺血预处理组（R组），右美托咪定组（D组），右美托咪定联合远隔缺血预处理组(DR组)；R组于麻醉诱导后行上肢缺血预处理，D组将盐酸右美托咪定以1 μg/kg负荷剂量泵注10 min后以0.41 μg/ (kg·h)注入至手术结束，DR组联合应用D组和R组两种方法；测主动脉阻断前（T₀）、体外循环结束时（T₁）和结束手术后（T₂）血浆肌钙蛋白I(cTnI)浓度。检测T₀和T₁ 时Bcl-2和Bax蛋白含量及计数心肌细胞凋亡指数（AI）。 结果 T₁和T₂时，与对照组比较，各组血浆cTnI均降低(P<0.05)。与阻断主动脉前相比，体外循环结束后4组心肌组织Bcl-2、Bax蛋白值含量和AI均升高，Bcl-2/Bax下降（P<0.05）；与C组比较，D组、R组和DR组Bcl-2、Bcl-2/Bax均增高，Bax和AI降低（P<0.05）；与R组、D组比较，DR组Bcl-2、Bcl-2/Bax升高，Bax和AI降低（P<0.05）。 结论 右美托咪定与远隔缺血预处理均能减轻MI/RI，二者联合作用优于单独使用，其机制可能与抑制细胞凋亡有关。     

Role of ischemic preconditioning on ischemia-reperfusion injury of the lung.

STUDY OBJECTIVES: Ischemia-reperfusion injury of the lung frequently occurs after cardiopulmonary bypass, after pulmonary thromboembolectomy, and especially during lung transplantation. The protective effects of preconditioning on the heart, liver, bones, and various other organs have been previously evaluated. In this comparative study, we used isolated guinea pig lungs to show the effects of preconditioning on lung ischemia. METHODS: The lungs (n = 10 in each group) were mounted on a modified Langendorff perfusion apparatus and perfused by Krebs-Henseleit solution for 30 min. We applied an ischemic preconditioning (5 min ischemia + 5 min perfusion, two times) in the experimental group. After 3 h of normothermic ischemia, the lungs were reperfused for 30 min. Pulmonary artery pressures and malondialdehyde (MDA) and glutathione (GSH) levels of the tissue and the perfusate were measured before and after the ischemic period and also at the end of reperfusion. Electron microscopic evaluation was done on randomly selected lungs of three animals in each group at the end of the experiment. RESULTS: Both MDA and GSH levels of tissue and perfusate decreased in the experimental group after reperfusion, although the reduction in GSH levels did not reach statistical significance. The increase in pulmonary artery pressure was lower in the preconditioning group after reperfusion. CONCLUSIONS: Our data showed that ischemic preconditioning of the lung may have a protective effect in ischemic-reperfusion injury.     

缺血预适应对大鼠肺缺血再灌注中NF-κB表达的影响

目的研究缺血预适应(IP)对缺血再灌注(I/R)后在体鼠肺脏NFκB表达的影响,探讨IP减轻肺脏I/R损伤的可能机制及NFκB的作用。方法雄性SD大鼠36只,随机分为3组假手术(Sham)组,缺血再灌注(I/R)组,缺血预适应(IP)组。I/R组开胸后,建立在体肺脏I/R损伤模型。在此基础上,IP组于缺血开始前,应用3个循环的5min缺血 5min灌注进行IP处理。用免疫组化法观察肺脏NFκB的表达,同时测定肺脏湿重/干重(W/D)比值,电镜下观察肺脏超微结构的改变,光镜下HE染色观察肺脏的病理形态学变化。结果IP组和I/R组相比肺脏NFκB表达有显著性差异(P<0.01),肺脏超微结构损害和肺水肿程度明显减轻。结论IP可抑制I/R损伤时肺组织中NFκB的表达,从而减轻肺脏超微结构损害和肺水肿程度,减轻肺I/R损伤。     

丹参多酚酸盐预处理对大鼠心肌缺血再灌注损伤的防护作用

目的:观察丹参多酚酸盐预处理对大鼠心肌缺血再灌注损伤的防护作用。方法:将健康成年雄性SD大鼠40只随机分为假手术组(S组)、缺血再灌注组(I/R组)、低剂量组(LD组)和高剂量组(HD组)。采用结扎大鼠左冠状动脉前降支(LAD)30min、恢复灌注120min制备大鼠心肌缺血再灌注模型。分别于药物输注前(T1),LAD阻断后30min(T2),LAD开放后30min(T3)、3h(T4)、6h(T5)、24h(T6)共6个时点测定血清一氧化氮合酶(NOS)、超氧化物岐化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GPX)、肌酸磷酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)及肌钙蛋白(cTnI)水平。结果:与I/R组比较,LD组和HD组血清CK-MB、LDH、cTnI、MDA及NOS水平显著降低,SOD与GPX含量显著上升(均P<0.05)。结论:丹参多酚酸盐预处理对大鼠心肌缺血再灌注损伤具有较好的防护作用。     

缺血预处理对移植肝缺血再灌注损伤中细胞凋亡的影响

目的 探讨细胞凋亡在移植肝缺血再灌注损伤中的作用及缺血预处理对其影响。方法 通过对移植肝进行 因预处理,用全自动生化分析仪检测肝功能、比色法测定移植肝组织的ＭＤＡ、用流式细胞仪结合原位标记技术检测细胞调７亡。结果 移植肝再灌注后血中ＡＳＴ、ＡＬＴ、ＬＤＨ和肝组织中ＭＤＡ均明显升亮,肝细胞调亡明显增加,经缺血预处理后,血中ＡＳＴ,ＡＬＴ,ＬＤＨ和肝组织中ＭＤＡ均降低,肝细胞调亡亦明显减少,结论 缺血     

脑缺血预处理对脑缺血再灌注大鼠血脑屏障通透性和基质金属蛋白酶-9表达的影响

目的 探讨脑缺血预处理(ischemic preconditioning,IP)对脑缺血再灌注大鼠血脑屏障通透性和基质金属蛋白酶-9(matrix metalloproteinase-9,MMP-9)表达的影响.方法 154只Wistar大鼠随机分为假手术组(14只)、非缺血预处理(non-ischemic preconditioning,NIP)组(70只)和IP组(70只),后两组再随机分为5个亚组,每组14只.线栓法建立大脑中动脉闭塞模型,缺血预处理10 min,分别在IP后1、3、7、14和21 d进行再次缺血2 h再灌注22 h.采用2,3,5-氯化三苯基四氮唑(2,3,5-triphenyltetrazolium chloride,TTC)染色测定脑梗死体积,通过测定渗出血管外的伊文思蓝(Evans blue,EB)含量评价血脑屏障通透性,采用于湿重法评价脑水肿程度,免疫组化染色和原位杂交法检测MMP-9蛋白和mRNA表达.结果 与NIP组相应亚组比较,IP组缺血预处理1、3和7 d亚组神经功能缺损评分显著降低,脑梗死体积显著缩小,EB含量和脑水含量显著降低,MMP-9蛋白和mRNA表达均显著下调(P＜0.05或P＜0.01).IP组1、3和7 d亚组梗死体积和MMP-9 mRNA表达较IP组14 d和21 d亚组显著缩小或下调,3 d和7 d亚组EB含量、脑水含量和MMP-9蛋白表达较其他亚组显著降低,其中以3 d亚组降低最显著(P＜0.05).结论 缺血预处理诱导的血脑屏障通透性改变和MMP-9表达下调在脑缺血耐受中发挥着重要作用.     

脑缺血预处理对脑缺血再灌注大鼠血脑屏障通透性和基质金属蛋白酶-9表达的影响

Objective To investigate the effects of ischemic preconditioning (IP) on blood-brain barrier permeability and matrix metalloproteinase-9 expression after cerebral ischemia reperfusion in rats.Methods A total of 154 Wistar rats were randomly divided into sham operation (n = 14),non-ischemic preconditioning (NIP,n = 70),and IP (n = 70) group.The latter two groups were redivided into 5 subgroups (n = 14 in each subgroup).A middle cerebral artery occlusion model was induced by intraluminal suture method.After 10 minutes IP,re-ischemia for 2 hours and reperfusion for 22 hours were performed at day 1,3,7,14,and 21,respectively.The infarct volume was detected using 2,3,5-triphenyltetrazolium chloride (TTC)staining.The BBB permeability were evaluated by measuring the content of the extravascular exudation of Evan's blue (EB).The degree of cerebral edema was evaluated using the wet-dry weight method.MMP-9 protein and mRNA expression were detected by immunohistochemical staining and in situ hybridization.Results Compared to the corresponding subgroups in the NIP group,the neurological deficit scores,infarct volume,EB content,and brain water content were decreased significantly,and MMP-9 protein and mRNA expression were down-regulated significantly in the day 1,3,and 7 subgroups in the IP group (P ＜ 0.05 or P ＜ 0.01 ).The infarct volume and MMP-9 mRNA expression of the day 1,3,7 subgroups in the IP group were more significantly reduced or down-regulated than those of the day 14 and21 subgroups in the IP group.The EB content,brain water content,and MMP-9 protein expression of the day 3 and 7 subgroups were more significantly lower than those in other subgroups.Among them,they were decreased most significantly in the day 3 subgroup (P ＜ 0.05).Conclusions The changes of IP-induced BBB permeability and the down-regulated MMP-9 expression may play important roles in cerebral ischemic tolerance.     

Ischemic preconditioning ameliorates intestinal injury induced by ischemia-reperfusion in rats

AIM: To evaluate preventative effects of ischemic preconditioning(IP) in a rat model of intestinal injury induced by ischemia-reperfusion(IR).METHODS: Male Sprague-Dawley rats(250-300 g) were fasted for 24 h with free access to water prior to the operation.Eighteen rats were randomly divided into three experimental groups: S group(n = 6),rats were subjected to isolation of the superior mesenteric artery(SMA) for 40 min,then the abdomen was closed; IRgroup(n = 6),rats were subjected to clamping the SMA 40 min,and the abdomen was closed followed by a 4-h reperfusion; IP group(n = 6) rats underwent three cycles of 5 min ischemia and 5 min reperfusion,then clamping of the SMA for 40 min,then the abdomen was closed and a 4-h reperfusion followed.All animals were euthanized by barbiturate overdose(150 mg/kg pentobarbital sodium,i.v.) for tissue collection,and the SMA was isolated via median abdominal incision.Intestinal histologic injury was observed.Malondialdehyde(MDA),myeloperoxidase(MPO) and tumor necrosis factor(TNF)-a concentrations in intestinal tissue were measured.Intercellular adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 expression,as well as nuclear factor(NF)-κB activity and expression in intestinal tissue were also determined.RESULTS: Compared with the IR group,IP reduced IR-induced histologic injury of the intestine in rats(2.00 ± 0.71 vs 3.60 ± 0.84,P 0.05).IP significantly inhibited the increase in MDA content(5.6 ± 0.15 μmol/L vs 6.84 ± 0.18 μmol/L,P 0.01),MPO activity(0.13 ± 0.01 U/L vs 0.24 ± 0.01 U/L,P 0.01),and TNF-a levels(7.79 ± 2.35 pg/m L vs 10.87 ± 2.48 pg/m L,P 0.05) in the intestinal tissue of rats.IP also markedly ameliorated the increase in ICAM-1(204.67 ± 53.27 vs 353.33 ± 45.19,P 0.05) and VCAM-1(256.67 ± 58.59 vs 377.33 ± 41.42,P 0.05) protein expression in the intestinal tissues.Additionally,IP remarkably decreased NF-κB activity(0.48 ± 0.16 vs 0.76 ± 0.22,P 0.05) and protein expression(320.23 ± 38.16 vs 520.76 ± 40.53,P 0.01) in rat intestinal tissue.CONCLUSION: IP may protect against IR-induced intestinal injury by attenuation of the neutrophilendothelial adhesion cascade via reducing ICAM-1 and VCAM-1 expression and TNF-a-induced NF-κB signaling pathway activity.     

Intermedin预处理对大鼠肾脏缺血再灌注损伤修复过程中细胞周期蛋白表达的影响

目的 观察Intermedin(IMD)预处理对大鼠肾脏缺血再灌注损伤(IRI)修复过程中细胞周期蛋白(cyclin)D1、cyclin E以及其依赖性激酶(CDKs)表达的影响,从而探讨IMD在这一过程中促进肾组织再生修复的作用机制.方法 健康雄性Wistar大鼠共144只,体质量180～220 g,随机分为对照组、IRI组、转空质粒组、转IMD组,每组36只.IRI组切除右肾后钝性分离左侧腹主动脉及肾动脉;转空质粒组、转IMD组大鼠切除右肾后,在六氟化硫微泡(声诺维)介导下将空质粒及IMD质粒转染入左肾;1周后分别制作肾脏IRI模型.每组于再灌注第1、2、3、4、7、14天时各取6只留取肾组织标本.检测各组肾组织中cyclin D1与CDK4,cyclinE与CDK2的表达.统计学处理采用单因素方差分析和t检验.结果 IRI组cyclin D1、cyclin E以及CDK4、CDK2于再灌注后第1、2、3、4、7天表达逐渐增高,第7天时到达最高峰,第14天时仍有少量表达,与对照组比较差异有统计学意义(F值=54.92,69.69,61.28,77.38,P均＜0.05).转IMD组上述指标在第1天即开始显著增高,第2、3、4、7天呈进行性下降,至第14天时恢复正常,与IRI组相比差异具有统计学意义(F值=54.92,69.60,61.28,77.38,P均＜0.05);转空质粒组与IRI组以上指标差异无统计学意义.结论 IMD预处理在大鼠肾脏缺血再灌注损伤后早期能使cyclinD1、cyclinE以及CDK4、CDK2的表达明显上调,这一机制可能促进细胞周期进展从而加快肾组织再生修复.     

白藜芦醇预处理对体外大鼠心肌缺血再灌注损伤的保护作用

目的:观察白藜芦醇预处理对体外大鼠缺血再灌注心肌损伤的保护作用及其作用机制。方法:利用Langendorff灌注系统,建立体外大鼠心肌常温全心心肌缺血30min再灌注120min损伤模型。将56只雄性SD大鼠随机分为4组(每组14只):缺血再灌注损伤(IRI)组、白藜芦醇组、Nω硝基L精氨酸甲酯(LNAME)组、氨基胍(AG)组。检测各组的心功能、心肌一氧化氮合酶(NOS)同工酶(NOSi)活性、一氧化氮(NO)的含量、丙二醛的含量、心肌梗死面积以及心肌细胞凋亡指数。结果:与IRI组相比,白藜芦醇组左室发展压(LVDP)、左室压力上升和下降最大变化速率(±dp/dtmax)明显改善(P<0.05或0.01);心肌梗死面积、心肌细胞凋亡指数、心肌丙二醛含量显著降低(P<0.01);心肌NOSi活性和NO含量显著升高(P<0.01)。LNAME组和AG组LVDP和±dp/dtmax显著低于白藜芦醇组(P<0.05或P<0.01);心肌梗死面积、心肌细胞凋亡指数、心肌丙二醛含量显著升高(P<0.01);心肌NOSi活性和NO含量显著降低(P<0.01)。结论:白藜芦醇对体外大鼠IRI具有保护作用,其机制可通过提高心肌NOSi活性,促进NO产生而介导的。