缺血后适应对大鼠局灶性脑缺血再灌注后谷氨酸的影响

目的:研究缺血后适应对大鼠局灶性脑缺血再灌注后谷氨酸(Glu)浓度变化的影响。方法:建立大鼠大脑中动脉阻塞(middle cerebral artery occlusion,MCAO)模型,将36只雄性SD大鼠随机分为假手术(Sham)组、脑缺血再灌注(I/R)组和缺血后适应(I Postcond)组,每组12只。应用高效液相色谱检测缺血脑组织匀浆Glu浓度。结果:局灶脑缺血再灌注6 h后,I Postcond组Glu浓度相较I/R组明显降低(P<0.01),局灶脑缺血再灌注24 h后,I Postcond组Glu浓度较I/R组低,但两者差异亦无显著性(P>0.05)。结论:本研究表明,I Postcond能够减轻MCAO大鼠模型中I/R损伤。细胞间隙Glu清除的加速可能是其重要保护机制之一。     

Neuroprotective properties of prostaglandin I2 IP receptor in focal cerebral ischemia

We and others have identified that inhibition of cyclooxygenase might not be the optimal approach to limiting brain damage after stroke. Now we are investigating the unique properties of the various prostaglandin receptors to determine whether blocking those that mediate toxicity or stimulating those that reduce toxicity will improve neurological outcomes. Here, we determined the respective contribution of the prostaglandin I₂ (PGI₂) receptor in transient middle cerebral artery (MCA) occlusion (tMCAO) and permanent MCAO (pMCAO) preclinical stroke models by using male wildtype (WT) and IP receptor knockout (IP^−/−) C57Bl/6 mice. In addition, we investigated the putative preventive and therapeutic effects of the IP receptor agonist beraprost. The infarct volumes and neurological deficit scores (NDS) were significantly greater in IP^−/− than in WT mice after both tMCAO and pMCAO. Interestingly, beraprost pretreatment (50 or 100 μg/kg p.o.) 30 min before tMCAO and post-treatment (100 μg/kg p.o.) at 2 or 4.5 h of reperfusion significantly reduced the neurological deficit score and infarct volume in WT mice. Post-treatment with beraprost (100 μg/kg p.o.) 4.5 h after pMCAO also significantly decreased neurological deficits and infarct volume in WT mice. Together, these novel findings suggest for the first time that PGI₂ IP receptor activation can attenuate anatomical and functional damage following ischemic stroke.     

NADPH氧化酶与脑缺血/再灌注损伤

氧化应激是发生脑缺血/再灌注(ischemia/reperfusion,I/R)损伤的重要机制.近来研究发现,还原型烟酰胺腺嘌呤二核苷酸磷酸(nicotinamide adenine dinucleotide phosphate,NADPH)氧化酶产生的活性氧对脑I/R后的氧化应激起到重要的作用.一些方法(如常压高氧、缺血后处理)和一些药物(如罗布麻宁、替米沙坦、桦木酸、加兰他敏、雷公藤红素等)可以NADPH氧化酶为靶点治疗脑I/R损伤.     

开颅法制作大鼠局灶性脑缺血再灌注模型的改良研究

目的:改良传统的开颅造模法,建立一种稳定、可靠的大鼠脑缺血再灌注模型。方法:20只SD大鼠随机分为假手术与缺血再灌注组,每组10只,分别行假手术操作及改良模型制作。改良模型为,大鼠开颅后暴露左侧大脑中动脉(middle cerebral artery,MCA),将直径0.12 mm的不锈钢丝放置于MCA下,近其主干,钢丝两端架于颞骨表面120 min,撤去钢丝即再灌注。假手术仅暴露MCA,不进行缺血及再灌注。大鼠再灌注24 h,通过神经功能缺失评分,TTC染色,神经元计数及病理形态学的方法对模型进行评价。结果:改良后的造模成功率为100%,梗死灶位于额、顶叶皮层,病理形态学表现为典型的缺血性改变,正常神经元数减少(P0.01)。神经功能缺失评分1.3±0.5,脑梗死体积比率为5.32%±1.28%,与假手术组相比均有统计学意义(P0.01)。结论:这一改良模型阻断及恢复MCA血流明确,梗死灶的大小、位置稳定,死亡率低,为脑缺血再灌注机制的研究及治疗方法的探讨提供了有益帮助。     

橄榄苦苷对大鼠局灶性脑缺血再灌注损伤和炎性反应的作用

目的:探讨橄榄苦苷(OE)对大鼠局灶性脑缺血/再灌注损伤和炎性反应的作用。方法:雄性SD大鼠随机分为假手术组(Sham组)、溶媒处理组(Vehicle组)和OE处理组(OE组)。用线栓法制作大脑中动脉脑缺血/再灌注(MCAO/R)模型。TTC染色检测脑梗死体积,免疫组化法检测缺血侧大脑皮层髓过氧化物酶(myeloperoxidase,MPO)和肿瘤坏死因子(TNF-α)表达,Western Blot法检测基质金属蛋白酶-9(matrix metallopeptidase 9,MMP9)及基质金属蛋白酶-2(matrix metallopeptidase 2,MMP2)的表达。结果:(1)Vehicle组大脑缺血侧有明显的梗死灶,而OE处理组脑梗死体积明显有所缩小(P0.01)。(2)Vehicle组MPO和TNF-α表达与Sham组相比显著提高(P0.01),而OE组两者的表达较Vehicle组明显降低(P0.01,P0.05)。(3)Western Blot显示:Vehicle组MMP2、MMP9的表达水平较Sham组显著提高,而OE处理下调两者表达(P0.01,P0.05)。结论:OE可能通过抑制炎性反应保护脑缺血再灌注损伤。     

银杏叶提取物对局灶性脑缺血再灌注不同时段的大鼠脑组织GFAP的影响

目的观察银杏叶提取物(extract of Ginkgo biloba,EGB)对大鼠局灶性脑缺血再灌注梗死区胶质纤维酸性蛋白(GFAP)表达的影响。方法采用改良线栓法建立大鼠大脑中动脉阻塞脑缺血再灌注模型。观察再灌注1～4d里大鼠神经功能缺损程度并应用免疫组织化学法、Metamoph图像分析系统对结果进行分析。结果EGB药物组神经功能评分较缺血再灌组好(P<0.05),GFAP阳性细胞于脑缺血2h再灌注24h后即已出现,48、72、96h阳性细胞表达量增加,其中以72h为最多,EGB可抑制缺血后GFAP的表达(P<0.05)。结论局灶性脑缺血后可诱导脑组织GFAP表达增强,EGB可抑制脑缺血再灌注后星形胶质细胞GFAP的高表达,提示EGB对缺血诱导的星形胶质细胞活化具有抑制作用,可能对脑缺血损伤的恢复起重要作用。     

白藜芦醇对大鼠脑缺血再灌注损伤后突触素表达的影响

目的探讨白藜芦醇对大鼠脑缺血再灌注损伤后突触素表达的影响。方法 72只SD雄性大鼠随机分成假手术组(Sham)、缺血对照组(Con)和白藜芦醇组(Res),每组24只。脑缺血3h后腹腔注射白藜芦醇或无水乙醇,连用7d。脑缺血24h时,TTC法测量脑梗死体积,干湿称重法检测脑含水量。缺血24h、7d、14d分别行Bederson神经功能缺损评分,免疫组织化学法及Western blotting检测突触素蛋白的表达。结果 TTC染色显示,缺血对照组和白藜芦醇组脑梗死体积较假手术组高(P0.05),而白藜芦醇组较缺血对照组显著减小(P0.05)。脑含水量检测显示,缺血对照组和白藜芦醇组较假手术组明显增高(P0.05),但白藜芦醇组较缺血对照组显著降低(P0.05)。神经功能缺损评分显示,24h、7d、14d缺血对照组和白藜芦醇组显著高于假手术组(P0.05),但白藜芦醇组较缺血对照组显著降低(P0.05)。免疫组织化学显示,缺血对照组24h时脑缺血皮质突触素阳性表达减少,7d、14d时逐渐增加,但均较假手术组显著减少;白藜芦醇组各时间点均较缺血对照组明显增加,14d增加更明显。Western blotting显示,缺血对照组24h、7d、14d脑缺血区皮质突触素蛋白表达较假手术组显著降低(P0.05),但7d、14d时逐渐增加;白藜芦醇组各时间点较缺血对照组显著增强(P0.05),14d时增加更显著。结论白藜芦醇治疗可增强脑缺血大鼠突触素的表达,改善神经功能。     

红景天苷对局灶性脑缺血再灌注大鼠突触超微结构的影响

目的研究红景天苷对局灶性脑缺血/再灌注损伤后突触结构和数密度的变化。方法采用线栓法制造大鼠大脑局灶缺血(2h)/再灌注模型(I/R模型),于灌注后1d、3d、7d、14d时间点断头取脑,电镜观察突触结构和数密度的变化。结果I/R模型组数目减少,7d降至最低,14d突触数目回升;突触结构随再灌注时间延长损伤加重,14d有所恢复;红景天组突触损害程度减轻,突触数目增加(P<0.05),突触数密度恢复的时间提早至7d。结论红景天苷可以减轻脑缺血再灌注后突触的损伤,易化突触可塑性。     

水通道蛋白-4在大鼠急性脑缺血再灌注脑组织中的表达

目的:探讨水通道蛋白-4(AQP4)在急性脑缺血再灌注脑组织中的表达规律。方法:线栓法建立右侧大脑中动脉栓塞(MCAO)模型,分为假手术组、栓塞组和再灌注组。对脑组织病理观察、TTC染色,免疫组织化学、原位杂交组织化学、荧光定量PCR和免疫印迹检测。结果:栓塞组在右侧基底节区见细胞器肿胀、细胞体积增大,但细胞膜和血脑屏障结构完整,TTC染色缺血面积明显增加。所有再灌注组右侧基底节区的细胞肿胀减轻,再灌注早期组可见轻度血管源性水肿,TTC染色缺血面积逐渐缩小。AQP4基因和蛋白的表达量明显下降,分别与栓塞组比较均存在显著性差异。再灌注后各组AQP4基因和蛋白表达明显下降,但均高于假手术组。结论:无论是脑缺血或是再灌注,AQP4的表达均与细胞内水肿的程度一致,再灌注早期可出现血管源性水肿,再灌注越早脑细胞越容易恢复正常。     

Rapamycin alleviates brain edema after focal cerebral ischemia reperfusion in rats

Brain edema is a major consequence of cerebral ischemia reperfusion. However, few effective therapeutic options are available for retarding the brain edema progression after cerebral ischemia. Recently, rapamycin has been shown to produce neuroprotective effects in rats after cerebral ischemia reperfusion. Whether rapamycin could alleviate this brain edema injury is still unclear. In this study, the rat stroke model was induced by a 1-h left transient middle cerebral artery occlusion using an intraluminal filament, followed by 48?h of reperfusion. The effects of rapamycin (250?μg/kg body weight, intraperitoneal; i.p.) on brain edema progression were evaluated. The results showed that rapamycin treatment significantly reduced the infarct volume, the water content of the brain tissue and the Evans blue extravasation through the blood–brain barrier (BBB). Rapamycin treatment could improve histological appearance of the brain tissue, increased the capillary lumen space and maintain the integrity of BBB. Rapamycin also inhibited matrix metalloproteinase 9 (MMP9) and aquaporin 4 (AQP4) expression. These data imply that rapamycin could improve brain edema progression after reperfusion injury through maintaining BBB integrity and inhibiting MMP9 and AQP4 expression. The data of this study provide a new possible approach for improving brain edema after cerebral ischemia reperfusion by administration of rapamycin.     

Modulation of the balance between cannabinoid CB(1) and CB(2) receptor activation during cerebral ischemic/reperfusion injury

Cannabinoid receptor activation has been shown to modulate both neurotransmission (CB(1)) and neuroinflammatory (CB(2)) responses. There are conflicting reports in the literature describing the influence of cannabinoid receptor activation on ischemic/reperfusion injury. The goal of this study was to evaluate how changing the balance between CB(1) and CB(2) activation following cerebral ischemia influences outcome. CB(1) and CB(2) expression were tested at different times after transient middle cerebral artery occlusion (MCAO) in mice by real-time RT-PCR. Animals subjected to 1 h MCAO were randomly assigned to receive different treatments: a CB(1) antagonist, a CB(2) antagonist, a CB(2) agonist, a CB(1) antagonist plus CB(2) agonist, a CB(2) antagonist plus CB(2) agonist or an equal volume of vehicle as control. Cerebral blood flow was continuously monitored during ischemia; cerebral infarction and neurological deficit were tested 24 h after MCAO. Cerebral CB(1) and CB(2) mRNA expression undertook dynamic changes during cerebral ischemia. The selective CB(1) antagonist significantly decreased cerebral infarction by 47%; the selective CB(2) antagonist increased infarction by 26% after 1 h MCAO followed by 23 h reperfusion in mice. The most striking changes were obtained by combining a CB(1) antagonist with a CB(2) agonist. This combination elevated the cerebral blood flow during ischemia and reduced infarction by 75%. In conclusion, during cerebral ischemia/reperfusion injury, inhibition of CB(1) receptor activation is protective while inhibition of CB(2) receptor activation is detrimental. The greatest degree of neuroprotection was obtained by combining an inhibitor of CB(1) activation with an exogenous CB(2) agonist.     

Protective effects of melatonin on testicular torsion/detorsion-induced ischemia–reperfusion injury in rats

Testicular torsion causes an enhanced formation of reactive oxygen species, which contributes to the pathophysiology of tissue damage. The aim of this study was to investigate the protective effect of melatonin on testicular torsion/detorsion-induced ischemia–reperfusion (I/R) injury. A total of 24 male Wistar albino rats were divided into three groups of 8 animals each: control, I/R, and I/R treated with melatonin. The ischemia period was 5 h and orchiectomy was performed after 5 h of detorsion. Melatonin (10 mg/kg, intraperitoneally [i.p.]) was administrated only once, 40 min prior to detorsion. Spermatogenesis and mean seminiferous tubule diameter (MSTD) were significantly decreased in the I/R groups were compared to the control group. Furthermore, the melatonin treated animals showed an improved histological appearance in the I/R group. Our data indicate a significant reduction in the activity of TUNEL; there was a rise in the expression of proliferating cell nuclear antigen (PCNA) and testosterone in testes tissue of the I/R group treated with melatonin therapy. Electron microscopy of the testes of the rats demonstrated that pretreatment with melatonin was particularly effective in preventing mitochondrial degeneration, dilatation of SER, and enlarged intercellular spaces in both Sertoli and spermatid cells in the I/R treated animals. We believe that further preclinical research into the utility of melatonin may indicate its usefulness as a potential treatment on testes injury after I/R in rats.     

补体C1q与C3c在脑缺血/再灌注损伤大鼠脑组织中的表达

目的观察脑缺血再灌注(I/R)损伤大鼠脑组织中补体C1q与C3c的表达,探讨补体反应与小胶质细胞在脑I/R损伤中的作用及其机制。方法 48只SD雄性大鼠随机分为正常对照组、假手术组、I/R模型24 h、72 h、7 d、15 d组,线栓法建立局灶性大脑中动脉闭塞再灌注模型。尼氏体染色观察神经元结构,免疫组化法检测CD11b以及C1q、C3c的表达水平。结果与sham组相比,I/R 24 h组脑组织尼氏体染色加深,随后染色反应减弱,尤以I/R 72 h组减少最为显著;I/R 24 h组脑组织CD11b表达增多且在I/R 72 h组达到峰值,随后逐渐减少,与sham组比较,全部模型组差异显著(P0.05);I/R 24 h组脑组织C1q与C3c急剧增多且在I/R 7 d组达到峰值,随后见下降趋势,全部模型组与sham组比较差异显著(P0.05)。结论脑I/R损伤大鼠脑组织中C1q、C3c与CD11b的表达呈正相关。提示脑I/R损伤后,启动了脑内固有免疫反应,补体C1q与C3c活化,同时激活小胶质细胞,在脑I/R损伤中起到保护或损伤作用。     

美满霉素联合栀子苷对大鼠局灶性脑缺血再灌注损伤的保护作用

目的:观察美满霉素联合栀子苷对大鼠缺血性脑损伤神经元凋亡的拮抗作用和对脑组织的保护作用。方法:SD大鼠随机分为假手术组、脑缺血再灌注组、美满霉素组、栀子苷组和美满霉素联合栀子苷组。用线栓法建立大鼠右侧局灶性脑缺血再灌注模型,在体分别观察美满霉素和栀子苷单一和两者联合干预缺血性脑损伤。TTC染色观察脑梗死面积,H-E染色观察海马神经元形态学的变化,TUNEL染色观察凋亡情况。结果:美满霉素和栀子苷均能有效促进脑损伤后海马组织的恢复并能拮抗神经元的凋亡,与脑缺血再灌注组相比差异具有统计学意义;两者联合应用较单一使用具有较好的效果。结论:美满霉素联合栀子苷对缺血性脑组织具有保护作用并能有效拮抗神经元的凋亡。     

内质网应激相关分子葡萄糖调节蛋白78及增强子结合蛋白同源蛋白在高血压大鼠全脑缺血海马区的表达变化

目的:观察血压正常大鼠和高血压大鼠全脑缺血再灌注后海马区CAAT/增强子结合蛋白同源蛋白(CHOP)、葡萄糖调节蛋白78(GRP78)的表达变化,探讨内质网应激在高血压增加脑缺血再灌注神经易损性中的作用.方法:60只雄性血压正常Wistar-Kyoto(WKY)大鼠随机分为假手术组(Sham)和全脑缺血再灌注组(I/R);另取30只雄性自发性高血压大鼠为高血压全脑缺血再灌注组(SHR+I/R).应用改良的Pulsineli 4血管阻断(4-VO)法制作全脑缺血再灌注模型.各组分别在术后6、24、48 h,H-E染色观察海马区神经细胞形态变化;免疫组织化学和免疫印迹检测海马区CHOP、GRP78的表达;48 h八臂迷宫检测动物行为学变化.结果:与Sham组比较,I/R组各时间点存活神经元数量降低;GRP78表达增高,24 h达高峰;CHOP表达增高,24 h达高峰,高表达持续至48 h;与I/R组比较,SHR+ IR组各时间点存活神经细胞数量降低;GPR78表达6h增高,24、48h显著减少;6、24 h CHOP表达增高,48 h明显减少;八臂迷宫结果显示SHR+I/R组与I/R组比较,各检测指标变化差异有统计学意义.结论:高血压可增加脑缺血再灌注神经易损性,与加重缺血再灌注后GRP78表达下降、CHOP活体表达增高有关.     

动员造血干细胞对局灶性缺血再灌注大鼠脑组织C-FOS mRNA表达的影响

目的探讨应用粒细胞集落刺激因子(G-CSF)动员自体造血干细胞(HSC)对大脑中动脉栓塞/再灌注大鼠(MCAO/R)脑组织C-FOSmRNA表达的影响。方法制作MCAO/R模型;免疫组化双标记法鉴定HSC向神经元样细胞分化;RT-PCR法检测C-FOSmRNA表达水平。结果模型 G-CSF组再灌注后24 h出现CD34/Brdu双标记,48 h时双标记最为显著;再灌注后48 h出现CD34/NSE双标记。模型组各时间点C-FOSmRNA表达显著高于假手术组;G-CSF致再灌注48 h后C-FOSmRNA表达显著下调。结论应用G-GSF动员大鼠自体HSC可促进脑缺血再灌注损伤修复,调节C-FOSmRNA表达水平可能为其作用机制之一,而部分HSC来源的细胞分化为神经元样细胞可能参与缺血损伤修复过程。     

红景天苷对局灶性脑缺血再灌注大鼠神经生长相关蛋白的影响

目的研究红景天苷对局灶性脑缺血/再灌注损伤(I/R)后神经生长蛋白(GAP-43)表达的影响。并探讨其可能的机制。方法Wistar大鼠随机分为假手术组、I/R模型组和红景天苷组,采用线栓法制造大鼠大脑中动脉阻塞/再灌注(MCAO/R)模型,MCAO2h后恢复再灌注。用免疫组化方法检测再灌注后1d、3d、7d、14d、21d的与个时间点GAP-43的表达。结果红景天苷明显减小梗死灶范围,梗死灶周围皮质神经元损伤明显减轻。假手术组中枢神经系统GAP-43表达较少,I/R组GAP-43阳性表达,在术后1d开始增高,3d表达最强,高水平维持到7d,14d明显降低,但未降至正常水平。红景天苷组各个时间点GAP-43阳性表达强度均显著高于I/R对照组(P<0.05)。结论红景天苷能提高脑缺血/再灌注后GAP-43的表达,促进轴突生长,易化脑缺血再灌注损伤后神经可塑性。     

脑心清对脑缺血再灌注损伤模型大鼠的保护机制

文题释义： 缺血再灌注氧化应激：在脑部缺血再灌注的过程中,脑组织内活性氧浓度增加/抗氧化活性降低,从而积累大量的活性氧,并进一步的诱导中性粒细胞炎性浸润,蛋白酶分泌增加,随之产生大量氧化中间产物,进一步刺激脑组织的损伤。细胞焦亡：细胞的程序性死亡方式,其主要依赖半胱天冬酶1(caspase-1)发生,当细胞出现焦亡现象时,会有大量的促炎因子释放,相比于细胞凋亡及坏死,细胞焦亡的过程更为剧烈。细胞焦亡会快速的形成质膜孔洞,直接介导细胞肿胀、坏死。并大量释放细胞内容物,并进一步刺激氧化应激反应的发生。其为脑缺血再灌注过程中的重要研究热点之一。 背景：脑心清胶囊用于脑缺血再灌注损伤的治疗由来已久,然而针对其作用机制的深入研究则相对较少。 目的：应用分子生物学手段考察脑心清胶囊对脑缺血再灌注损伤沙鼠模型的治疗作用。 方法：实验方案经辽宁中医药大学动物实验伦理委员会批准(批准号为21000092017072)。将80只雄性蒙古沙鼠随机分为假手术组、模型组、脑心清组及脑络通组,后3组沙鼠应用无创微动脉夹同时夹闭双侧颈总动脉5 min后松开,建立脑缺血再灌注损伤模型;假手术组不夹闭双侧颈总动脉。术后次日开始假手术组正常饲养,模型组灌服同体积的生理盐水,脑心清组按照100 mg/(kg•d)灌胃给药,脑络通组按照100 mg/(kg•d)灌胃给药,连续给药21 d。在实验结束前1周进行水迷宫实验,实验结束后麻醉下处死沙鼠取脑组织。检测沙鼠的学习记忆功能、海马神经元、脑血管及对应的分子变化情况。 结果与结论：①同假手术组相比,模型组沙鼠学习能力显著下降。而脑心清组及脑络通组则可有效提升术后的学习能力下降趋势;②与模型组相比,脑心清组及脑络通组神经元显著增多,且排列较为整齐,细胞轮廓清晰,结构完整;③与模型组相比,脑心清组及脑络通组沙鼠的超氧化物歧化酶和乳酸脱氢酶活性,谷胱甘肽含量显著升高,丙二醛含量显著降低(P < 0.01);④与模型组相比,脑心清组及脑络通组沙鼠海马组织ASC、NLRP3和Caspase-1蛋白表达下调(P < 0.05);⑤与模型组相比,脑心清组及脑络通组沙鼠的白细胞介素18和白细胞介素1β含量明显降低(P < 0.01);⑥与模型组相比,脑心清组及脑络通组沙鼠的血小板内皮细胞黏附分子1阳性细胞明显增多,细胞间连接紧密;⑦与模型组相比,脑心清组及脑络通组沙鼠海马组织血小板内皮细胞黏附分子1和磷酸化内皮型一氧化氮合酶表达显著上调,一氧化氮含量显著升高(P < 0.01);⑧结果说明,脑心清胶囊可有效保护沙鼠的海马CA1区形态;脑缺血再灌注时伴有脑血管功能紊乱,脑心清胶囊可以保护脑血管功能,进而抑制脑缺血再灌注损伤。ORCID: 0000-0001-6646-9555(闵冬雨) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

二氧化硫对大鼠缺血再灌注心脏的损伤作用

目的观察二氧化硫(SO2)在心肌缺血再灌注损伤中的作用。方法大鼠心脏分为:I/R组,SO2组及天冬氨酸异羟肟酸(HDX)组。采用Langendorff离体心脏灌注模型。MacLab数据采集系统监测离体心脏功能。结果SO2组心功能恢复率明显低于I/R组(P<0.05,P<0.01);HDX组显著高于I/R组(P<0.05,P<0.01)。SO2组冠脉流液中乳酸脱氢酶(LDH)、肌酸激酶(CK)、谷氨酸-草酰乙酸转移酶(GOT)活性、肌红蛋白(Mb)含量及心肌丙二醛(MDA)、共轭双烯键(CD)含量及GOT活性显著高于I/R组(P<0.05,P<0.01);HDX组冠脉流液中上述指标明显低于I/R组(P<0.05,P<0.01)。SO2组心肌还原型谷胱甘肽(GSH)含量明显低于I/R组(P<0.05);HDX组心肌GSH含量显著高于I/R组(P<0.01)。结论SO2参与了大鼠心肌缺血再灌注损伤。增加心肌脂质过氧化及降低心肌还原型谷胱甘肽含量可能与SO2心肌损伤有关。