Sevoflurane postconditioning alleviates action potential duration shortening and L-type calcium current suppression induced by ischemia/reperfusion injury in rat epicardial myocytes

Background  It has been proved that sevoflurane postconditioning (SpostC) could protect the heart against myocardial ischemia/reperfusion injury, however, there has been few research focused on the electrophysiological effects of SpostC. The objective of the study was to investigate the effects of SpostC on action potential duration (APD) and L-type calcium current (I_{Ca, L}) in isolated cardiomyocytes.

Methods  Langendorff perfused SD rat hearts were randomly assigned to one of the time control (TC), ischemia/reperfusion (I/R, 25 minutes of ischemia followed by 30 minutes of reperfusion), and SpostC (postconditioned with 3% sevoflurane) groups. At the end of reperfusion, epicardial myocytes were dissociated enzymatically for patch clamp studies.

Results  Sevoflurane directly prolonged APD and decreased peak I_{Ca, L} densities in epicardial myocytes of the TC group (P <0.05). I/R injury shortened APD and decreased peak I_{Ca, L} densities in epicardial myocytes of the I/R group (P <0.05). SpostC prolonged APD and increased peak I_{Ca, L} densities in epicardial myocytes exposed to I/R injury (P <0.05). SpostC decreased intracellular reactive oxygen species (ROS) levels, reduced the incidence of ventricular tachycardia and ventricular fibrillation, and decreased reperfusion arrhythmia scores compared with the I/R group (all P <0.05).

Conclusions  SpostC attenuates APD shortening and I_{Ca, L} suppression induced by I/R injury. The regulation of APD and I_{Ca, L} by SpostC might be related with intracellular ROS modulation, which contributes to the alleviation of reperfusion ventricular arrhythmia.

     

Effect of anti-P-selectin monoclonal antibody on renal ischemia/rep erfusion injury in rats

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Combined postconditioning with ischemia and α7nAChR agonist produces an enhanced protection against rat myocardial ischemia reperfusion injury

Background  Inflammation is one of important mechanisms for myocardial ischemia reperfusion injury (IRI). Ischemia postconditioning (IPOC) can protect the heart against IRI by inhibiting inflammation, but its cardioprotection is weaker than that of ischemia preconditioning. Recently, the α7 subunit-containing nicotinic acetylcholine receptor (α7nAChR) agonist has shown anti-inflammatory effects in many diseases related to inflammation. This randomized controlled experiment was designed to evaluate whether combined postconditioning with IPOC and the α7nAChR agonist could produce an enhanced cardioprotection in a rat in vivo model of acute myocardial IRI.

Methods  Fifty Sprague-Dawley rats were randomly divided into five equal groups: sham group, control group, IPOC group, α7nAChR agonist postconditioning group (APOC group) and combined postconditioning with IPOC and α7nAChR agonist group (combined group). Hemodynamic parameters were recorded during the periods of ischemia and reperfusion. Serum concentrations of troponin I (TnI), tumor necrosis factor α (TNF-α) and high-mobility group box 1 (HMGB-1) at 180 minutes after reperfusion were assayed in all groups. At the end of the experiment, the infarct size was assessed from excised hearts by Evans blue and triphenyl tetrazolium chloride staining.

Results  As compared to the sham group, the infarct size in the other four groups was significantly increased, serum levels of TnI, TNF-α and HMGB1 in the control group and TNF-α, HMGB1 in the IPOC group were significantly increased. The infarct size and serum concentrations of TNF-α, HMGB1 and TnI in the IPOC, APOC and combined groups were significantly lower than those in the control group. As compared to the IPOC group, the infarct size in the combined group was significantly decreased, serum concentrations of TnI, TNF-α and HMGB1 in the APOC and combined groups were significantly reduced. Although the infarct size was significantly smaller in the combined group than in the APOC group, serum levels of TNF-α and HMGB1 were significantly higher in the combined group than in the APOC group.

Conclusions  In a rat in vivo model of acute myocardial IRI, combined postconditioning with IPOC and the α7nAChR agonist can produce enhanced protection against myocardial IRI by increasing the anti-inflammatory effect.

     

The Effect of Sleep Deprivation on Coronary Heart Disease

AbstractSleep deprivation (SD) has been associated with an increased morbidity and mortality of coronary heart disease (CHD). SD could induce autonomic nervous dysfunction, hypertension, arrhythmia, hormonal dysregulation, oxidative stress, endothelial dysfunction, inflammation and metabolic disorder in CHD patients. This paper reviewed the study results of SD in clinical trials and animal experiments and concluded that SD was associated with cardiovascular risk factors, which aggravated CHD in pathogenesis and outcomes.     

Effects of Acupuncture at Baihui(GV 20) and Zusanli(ST 36) on Peripheral Serum Expression of MicroRNA 124,Laminin and Integrin β1 in Rats with Cerebral Ischemia Reperfusion Injury

Objective:To explore the effects of acupuncture at Baihui(GV 20) and Zusanli(ST 36) on the peripheral serum expression of microRNA 124(miRNA 124),laminin and integrin β 1 in rats with cerebral ischemia reperfusion injury(CIRI).Methods:Seventy-two healthy male Sprague-Dawley rats were randomized into a model group,an acupuncture group,and a sham-operated group using a random digits table,with 24 rats per group.Each group was further randomly divided into 1-,3-,5-,and 7-day subgroups based on the reperfusion time according to a random digits table,with 6 rats in each subgroup.In the model and acupuncture groups,CIRI was induced using the thread occlusion method.Electroacupuncture stimulation was applied daily to GV 20 and left ST 36 for 20 min at the indicated time points after successful operations.Serum was sampled for detecting laminin and integrin β1 protein via enzyme-linked immunosorbent assay,and serum miRNA 124 was examined using quantitative polymerase chain reaction.Results:The serum level of miRNA 124 in the cerebral ischemia rats increased significantly,and the peak expression of miRNA 124 in both the model and acupuncture groups occurred at 3 days.The expression of miRNA 124 in the acupuncture group was higher than in the model group at the same time point(5.96 ±0.01 vs.3.11 ±0.04,P0.05).Laminin expression in serum from the cerebral ischemia group was higher than that in the sham-operated group.Compared with the model group,the level of laminin in the serum of the acupuncture group was significantly lower at each time point,especially at the 3-day,and 7-day time points(589.12±3.57 vs.793.05 ± 5.28,and 600.53 ±3.05 vs.899.06 ±5.74,P0.05).The level of integrin β 1 in the serum from the acupuncture group was lower than that in the model group particularly at the 3-day and 7-day time points(208.66 ±0.95 vs.280.83 ±1.77,and212.36 ±0.95 vs.316.77±2.42,P0.05).Additionally,the model group and the acupuncture group showed dual peaks of integrin β 1 and laminin expression at 3-day and 7-day.Conclusions:Acupuncture at GV 20 and ST 36 in rats alleviated CIRI and was associated with upregulated expression of miRNA 124 and with downregulated expression of integrin β 1 and laminin in peripheral serum.These changes may represent one of the mechanisms underlying acupuncture's attenuation of CIRI.     

Neutroprotective efficacy of sodium tanshinone B on hippocampus neuron in a rat model of focal cerebral ischemia

<正>Objective:To investigate the protective effects of sodium tanshinone B(STB) on brain damage following focal ischemia-reperfusion(l/R) injury through interfering with N-methyl-D-aspartic acid receptor(NMDAR) and excitatory and inhibitory amino acids,and evaluate the potential mechanisms of the neuroprotective activity of STB.Methods:Transient forebrain ischemia was induced by middle cerebral artery occlusion(MCAO).The rats were randomized into a sham operated group,a model group(l/R) and three STB different dose groups.Rats were pretreated with STB at the doses of 4,8,16 mg/kg(STB_1,STB_2,STB_3) for 3 days before MCAO.The expression of NMDAR1 was detected by immunohistochemistry and Western blotting. The concentrations of glutamate and y -aminobutyric acid(GABA) were analyzed using high performance liquid chromatography.Results:STB treatment reduced neurological defect scores,cerebral infarction volume and brain water content.The levels of NMDAR1 were significantly higher in the l/R and STB,groups than that of the sham and the STB_3 groups(P0.01).Optical density of NMDAR1 was significantly increased in cornu ammonis(CA)1 region of the l/R group(P0.05).STB treatment reduced NMDAR1 optical density in the CA1 region(P0.01).The levels of glutamate were significantly lower in the hippocampus in the STB_3 group than that of the l/R,STB,and STB_2 groups(P0.01).Conclusion:Preconditioning with STB appears to be a simple and promising strategy to reduce or even prevent cerebral l/R injury and has potential for future clinical application.     

Management of cerebral ischemia due to Takayasu’s arteritis

Objective To explore the management of cerebral ischemia caused by Takayasu’s arteritis. Methods Ninety-three cases treated from June 1984 to September 1999 at the General Post &amp; Telecom Hospital, the Sir Run Run Shaw Hospital, the First Af filiated Hospital of Zhejiang University, the Second Medical College of Beijing University, Beijing An Zhen Hospital, and the Beijing Union Medical College Hosp ital, including 10 men and 83 women, were reviewed.Of the 93 cases, bypasses f rom the ascending aorta to the axillary or subclavian artery and from graft to t he carotid artery were performed in 47 cases.Subclavian to carotid bypass was performed in six cases.Percutaneous transluminal angioplasty (PTA) was used in five cases and stenting in one.Results Marked improvement was achieved in 30.3%, fair in 34.9%, improvement in 21.2 %, unchanged in 4.6%, and death in 9.0% before discharge; 30.6%, 38.8%, 16 .3%, 4.1%, and 2.0% respectively during a mean follow-up of 48 months, and r ecurrence requiring revision in 8.2%.Conclusion Patients with occlusive lesions of all four cervical arteries always have severe cerebral ischemia and their distal runoff is always unvisualised by angiography . However, we found by exploration that the internal carotid artery is patent in all but one patient. Therefore, an ascending aorta to carotid bypass is feasib le in most instances, and this can and should be done when the cerebral perfusio n is jeopardized at a time when the patient is in a stable or relatively stable condition. Unfortunately, the cerebral re-perfusion syndrome is still a serious and not completely solved problem.     

Surgical treatment of brachiocephalic vessel involvement in Takayasu’s arteritis

Background Takayasu＇s arteritis （TA） is a chronic idiopathic inflammatory disease that affects large and medium size arteries. The brachiocephalic trunk is the most frequently involved site in TA, and multi-vessel lesions are common. Surgical treatment includes vessel reconstruction surgery and percutaneous transluminal angioplasty （PTA）. Herein, we report our preliminary experience with surgical treatment of cerebral ischemia caused by cervical arterial lesions due to TA.Methods From January 2000 to December 2007, 38 patients with cerebral ischemia caused by cervical arterial occlusive lesions due to TA were treated surgically. There were three males and 35 females, with an age range of 15-42 years （mean 26.5 years）. All patients had operative repairs undertaken. Twenty eight patients received bypass operation and 10 patients received percutaneous transluminal angioplasty. One case with coronary stenosis received coronary artery bypass simultaneously. Patients were followed up for 11 months to eight years.Results There were no peri-operative deaths in cerebrovascular reconstruction patients. Symptoms of cerebral ischemia were improved or cured in 25 of 38 patients. There was a low incidence of cerebral reperfusion syndrome. Two patients died at five and seven years after surgery due to heart failure. Another 8 patients （20%） required further surgery for stenosis （5 patients） or anastomotic aneurysms （3 patients）. Percutaneous transluminal angioplasty was performed successfully for treatment of aortic and renal lesions. Repeated angioplasty for revascularization was performed in six PTA cases with restenosis after 5-24 months.Conclusions When cerebral perfusion has potential to be affected by TA, a definitive corrective procedure is advised when the patient is relatively stable. Although the recurrence rate is very high, percutaneous transluminal angioplasty is the first choice procedure. Bypass operation is optimal for brachiocephalic-vessel involvement in TA. Cerebral reperfusion syndrome can be avoided by careful selection of the operation method and improved post-operative treatment.     

Fenofibrate Pre-treatment Suppressed Inflammation by Activating Phosphoinositide 3 Kinase/Protein Kinase B(PI3K/Akt) Signaling in Renal Ischemia-Reperfusion Injury

The aim of this study was to investigate the possible beneficial effects of Fenofibrate on renal ischemia-reperfusion injury(IRI) in mice and its potential mechanism. IRI was induced by bilateral renal ischemia for 60 min followed by reperfusion for 24 h. Eighteen male C57BL/6 mice were randomly divided into three groups: sham-operated group(sham), IRI+saline group(IRI group), IRI+Fenofibrate(FEN) group. Normal saline or Fenofibrate(3 mg/kg) was intravenously injected 60 min before renal ischemia in IRI group and FEN group, respectively. Blood samples and renal tissues were collected at the end of reperfusion. The renal function, histopathologic changes, and the expression levels of pro-inflammatory cytokines [interleukin-8(IL-8), tumor necrosis factor alpha(TNF-α) and IL-6] in serum and renal tissue homogenate were assessed. Moreover, the effects of Fenofibrate on activating phosphoinositide 3 kinase/protein kinase B(PI3K/Akt) signaling and peroxisome proliferator-activated receptor-α(PPAR-α) were also measured in renal IRI. The results showed that plasma levels of blood urea nitrogen and creatinine, histopathologic scores and the expression levels of TNF-α, IL-8 and IL-6 were significantly lower in FEN group than in IRI group. Moreover, Fenofibrate pretreatment could further induce PI3K/Akt signal pathway and PPAR-α activation following renal IRI. These findings indicated PPAR-α activation by Fenofibrate exerts protective effects on renal IRI in mice by suppressing inflammation via PI3K/Akt activation. Thus, Fenofibrate could be a novel therapeutic alternative in renal IRI.     

褪黑素通过抑制挛缩减轻大鼠离体心脏的缺血再灌注损伤

目的 探讨褪黑素（Mel）抑制挛缩改善大鼠离体心脏缺血再灌注（IR）损伤的作用及机制。方法 采用Langendorff离体心脏灌流方法模拟缺血再灌注模型,40只SD大鼠按随机数字表法分为4组（10只/组）。正常对照组（Control）：正常灌注175 min;IR组：全心缺血45 min,再灌注120 min;Mel+IR组：用Mel（5 μmol/L）灌注1 min,全心缺血45 min,用Mel（5 μmol/L）再灌注5 min,Krebs-Henseleit液再灌注115 min;挛缩抑制剂2,3-丁二酮单肟（BDM）干预缺血再灌注组（BDM+IR）：用BDM（20 mmol/L）灌注1 min,全心缺血45 min,用BDM（20 mmol/L）再灌注5 min,KH液再灌注115 min。以心肌死亡面积、caspase-3活性、细胞色素c（cytochrome c）和cleaved caspase-3蛋白表达检测各组心肌损伤程度;以HE染色、冠脉流出液中乳酸脱氢酶（LDH）活性、肌钙蛋白（I cTnI）含量、左心室舒张末压（LVEDP）和电镜观察肌原纤维收缩带的形成评价各组心脏挛缩程度;检测心肌组织中ATP含量的变化。结果 与Control组相比,IR组心肌死亡面积、caspase-3活性、cytochrome c和cleaved caspase-3蛋白表达显著增加（P<0.01）;同时,冠脉流出液中LDH活性和cTnI含量明显增加,再灌注末LVEDP显著抬升,HE染色显示心肌纤维发生明显断裂,ELISA检测发现ATP含量显著降低（P<0.01）;另外,透射电镜结果表明IR组肌节过度收缩,形成明显的肌原纤维收缩带;而给予Mel和BDM处理后,可显著减小心肌死亡面积、aspase-3活性、cytochrome c和cleaved caspase-3蛋白表达,还可明显抑制LDH活性、cTnI含量和LVEDP,减少心肌纤维断裂,并增加胞内ATP含量;更为重要地是,Mel和BDM能减轻IR引起的肌节过度收缩,并抑制收缩带的形成。结论 Mel可通过抑制挛缩明显改善心肌缺血再灌注损伤,其机制可能与增加心肌细胞内ATP含量,减轻心肌机械性损伤引起的肌膜撕裂,减少细胞内容物的漏出有关。     

ERK1/2在缺血后适应减轻糖尿病小鼠心肌再灌注损伤中作用

目的 研究缺血后适应对糖尿病小鼠离体心脏缺血再灌注损伤的作用及细胞外信号调节激酶(ERK1/2)在缺血后适应心肌保护中的作用。方法将C57/BL小鼠随机分为6组:(1)空白对照组(N组);(2)缺血再灌注组(I/R组);(3)缺血后适应组(Post组);(4)糖尿病小鼠空白组(DN组);(5)糖尿病小鼠缺血再灌注组(D I/R组);(6)糖尿病小鼠后适应组(D post组)。观察后适应对心脏血流动力学、梗死心肌范围的影响及与ERK1/2表达水平的关系。结果与I/R组比较,左室舒张末期压力(LVDP)、左心室压力变化最大速率和最小速率(+dp/dtmax和-dp/dtmax)恢复率明显增加(P<0.05)。而D Post组与DI/R组比较上述变化均不明显(P>0.05)。Post组心肌梗死范围较I/R组显著减小(P<0.01),D Post与DI/R组比较差异无统计学意义(P>0.05)。各组小鼠体重、心重指数无明显差异。各组体外心脏组织中ERK1/2总蛋白表达无明显差异(P>0.05)。但与I/R组比较,Post组心肌磷酸化ERK1/2水平明显增加(P<0.01)。D Post组的心肌磷酸化ERK1/2水平与DI/R组比较未见明显增加(P>0.05)。结论缺血后适应能有效地减轻离体小鼠心肌再灌注损伤,改善心功能,而在糖尿病小鼠中,这种保护作用并不明显。糖尿病小鼠缺血后适应保护作用减弱可能与其不能明显激活ERK1/2有关。     

丹参素对大鼠离体心脏缺血再灌注心肌能量代谢的影响

SD大鼠随机分为正常灌流组和缺血再灌注组,对大鼠离体心脏进行Langendorff灌流。采用高效液相色谱法测定大鼠心肌组织中辅酶A、乙酰辅酶A及高能磷酸化合物含量,心肌组织中乳酸含量和灌流液中脂肪酸的含量采用试剂盒测定,观察给予丹参素和阳性药雷诺嗪后上述各指标的变化情况。结果表明,雷诺嗪能够增加心肌ATP储备,升高腺苷酸能荷值,降低心肌组织乳酸含量及含脂肪酸组乙酰CoA/CoA比值,抑制脂肪酸的氧化从而优化心肌能量代谢。丹参素可以使大鼠离体心脏ATP含量及腺苷酸能荷值升高,乳酸含量降低,对正常灌流组心肌组织乙酰CoA/CoA比值无明显影响,但可以降低添加脂肪酸的缺血再灌注组心肌组织乙酰CoA/CoA比值,提示丹参素对病理状态下心肌脂肪酸的氧化有一定的抑制作用,从而优化病理状态下的心肌能量代谢,发挥对缺血再灌注心肌的保护作用。     

Sevoflurane preconditioning and postconditioning attenuate apoptosis induced by ischemia-reperfusion in rat lung

Objective To investigate the effect of sevoflurane preconditioning and postconditioning on lung ischemia-reperfusion (IR) injury and apoptosis in rat.Methods Wistar rats were randomly assigned to four ...     

脂联素参与七氟醚预处理保护心肌缺血再灌注损伤后小鼠认知功能的机制研究

目的 探讨脂联素参与七氟醚预处理后心肌缺血再灌注（MIR）小鼠的认知功能保护作用的机制。方法 将野生健康成年SPF级雄性C57BL/6小鼠随机分为sham组、MIR-Control组、MIR-SevoPre组,每组10只。将健康成年SPF级雄性脂联素基因敲除（APN KO）小鼠随机分为KO-sham组、KO-MIR-Control组、KOMIR-Sevopre组、KO-MIR-Sevopre-AdipoRon组,每组10只。检测3组C57BL/6小鼠在模型复制或对照处理后12 h血浆的高、中和低分子量脂联素浓度;使用Morris水迷宫实验检测3组C57BL/6小鼠在模型复制或对照处理后24 h的游泳速率和潜伏期;检测4组APN KO小鼠在模型复制或对照处理后第1天、第2天、第4天的潜伏期。结果 3组C57BL/6小鼠模型复制后第1天、第2天和第4天的游泳速率比较,采用重复测量设计的方差分析,结果：(1)不同时间点的小鼠游泳速率无差异（P>0.05）;(2)3组小鼠游泳速率无差异（P>0.05）;(3)3组小鼠游泳速率的变化趋势无差异（P>0.05）。3组C57BL/6...     

丙泊酚预处理对大鼠离体心脏低温缺血常温再灌注损伤的保护作用

目的观察丙泊酚预处理对大鼠离体心脏低温缺血常温再灌注损伤的保护作用。方法采用Langendorff离体心脏灌注模型,60只SD大鼠离体心脏平衡20min后随机分为5组(n=12):空白对照组(Con组)于37℃用Krebs-Henseleit缓冲液(K-H液)持续灌注175min;缺血再灌注组(I/R组)于37℃用K-H液灌注40min,27℃缺血75min,37℃K-H液再灌注60min;丙泊酚预处理1组(P1组)、2组(P2组)和3组(P3组)分别在缺血前给予含50、100和150μmol/L丙泊酚预处理,预处理后同I/R组。观察平衡末(基础值)、缺血前及再灌注末的心率(HR)、左室舒张末压(LVEDP)、左室发展压(LVDP)、左室压力上升和下降速率最大值(±dP/dtmax);在平衡末、再灌注后1、10、20、30及60min分别取冠状动脉流出液,测定其中肌酸激酶(CK)和乳酸脱氢酶(LDH),再灌注末测定心肌组织中超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量;并测定再灌注后各组心肌梗死面积。结果P2组和P3组在再灌注后60min时HR、LVDP、±dP/dtmax、SOD活性均高于I/R组(P<0.05);而LVEDP、心肌梗死面积、MDA含量小于I/R组(P<0.05);P2组和P3组再灌注后各时间点冠状动脉流出液中CK及LDH值均明显低于I/R组相应时间点所测值(P<0.05)。结论100和150μmol/L丙泊酚预处理对大鼠心肌低温缺血再灌注损伤有保护作用。     

缺血预适应通过抑制TLR4/NF-KB信号通路保护大鼠心肌缺血再灌注损伤

目的:研究缺血预适应对大鼠心肌缺血再灌注损伤的保护作用是否由toll样受体4(TLR4)/NF-kB途径所介导,以及是否与促进降钙素基因相关肽(CGRP)释放有关.方法:结扎Sprague-Dawley大鼠左冠状动脉前降支60 min,复灌3h造成心肌缺血再灌注损伤.缺血预适应为结扎大鼠左冠状动脉前降支5 min,复灌5min,共4个周期.RT-PCR分析心肌TLR4 mRNA表达.免疫组织化学法分析心肌TLR4和NF-κB蛋白表达.同时,测定心肌梗死面积、血浆CGRP浓度和血清肌酸激酶活性.结果:缺血预适应显著减少心肌梗死面积,降低肌酸激酶活性,增高血浆CGRP水平.心肌缺血再灌注可显著上调TLR4和NF-κB表达,缺血预适应可抑制其作用.结论:缺血预适应通过抑制TLR4/NF-κB信号通路保护大鼠心肌缺血再灌注损伤,其作用与促进CGRP释放有关.     

抑制磷脂酰肌醇-3激酶通路减弱乙醇后处理的心肌保护作用

目的: 探讨抑制磷脂酰肌醇-3激酶(phosphatidylinositol 3-kinase,PI3K)途径是否减弱乙醇后处理的心肌保护作用。方法: 采用离体大鼠心脏Langendorff灌注方法,局部结扎冠状动脉左前降支30 min,再灌注120 min复制心肌缺血/再灌注模型。测定心室动力学指标和再灌注期间冠状动脉流出液中乳酸脱氢酶(lactate dehydrogenase,LDH)含量。结果: 与单纯缺血/再灌注相比,乙醇后处理明显促进了左心室发展压、左心室内压最大上升和下降速率、左心室做功量的恢复,降低再灌注期冠状动脉流出液中LDH的释放(P < 0.01);PI3K抑制剂渥曼青霉素减弱了乙醇后处理的作用,抑制了心室动力学指标的恢复(P <0.05~P < 0.01),LDH释放增多(P < 0.01)。结论: 抑制PI3K通路减弱了乙醇后处理的心肌保护作用。     

酸性液后处理对离体大鼠心肌缺血再灌注损伤保护作用的研究

目的通过心脏停搏液停搏的离体大鼠心脏模型,评价酸性缓冲液或者含有环孢素A（CsA）的酸性缓冲液是否具有心肌保护作用,其机制是否与抑制线粒体通透性转换孔开放有关。方法取SD大鼠心脏,建立离体Langendorff心肌缺血再灌注模型,随机分为3组（每组12只）。对照组（Con组）：经历平衡期20 min,St.ThomasⅡ停搏液灌注后常温缺血30min,KH缓冲液[pH：（7.4±0.5）]再灌注60 min。酸性后处理组（Low pH组）：再灌注开始3 min给予酸性KH缓冲液灌注（pH：6.8）。酸性缓冲液联合环孢素A后处理组（Low pH＋CsA组）：再灌注开始3 min给予含有0.2μmol/L环孢素A的酸性KH缓冲液灌注（pH：6.8）。检测各组血流动力学指标,Western blot法检测胞浆细胞色素C含量和总蛋白Bcl-2/Bax含量,线粒体肿胀液检测线粒体对Ca2＋的敏感度,TUNEL法检测心肌细胞凋亡。结果与Con组相比,Low pH组和Low pH＋CsA组在再灌注期间,左室发展压,等容收缩期左心室内压力上升的最大速率,等容舒张期左心室压力下降的最大速率以及心率明显优于Con组（P〈0.05）。Low pH组和Low pH＋CsA组的胞浆细胞色素C释放较Con组明显减少（P〈0.05）,同时Bcl-2/Bax明显高于Con组;再灌注5 min线粒体肿胀率测定,两组线粒体对Ca2＋诱导的通透性转换孔开放敏感度较Con组明显降低（P〈0.05）、且心肌细胞凋亡数明显低于Con组（P〈0.05）。结论酸性液后处理或联合环孢素A后处理能够减轻再灌注损伤引起的线粒体通透性增加,减少心肌细胞凋亡,改善心脏血流动力学功能。但添加环孢素A并不能增强其保护作用。酸性液后处理有可能作为一种新的心肌保护方法应用于心脏手术。