冠状血管内皮细胞与氧自由基致大鼠心肌损伤关系的研究

为探讨冠状血管内皮细胞在氧自由基致心肌损伤中的作用，采用电解法（恒流，5mA，2min）产生氧自由基（OFR），观察OFR对保留冠状血管内皮及去冠状血管内皮的Langendorff大鼠心脏心率（HR）、心律、冠脉灌注压（CPP）、左室内压峰值（LVSP）及左室舒张末压（LVEDP）、冠脉流出液中乳酸脱氢酶（LDH）含量、心肌组织中两二醛（MDA）及Na －K ATPase水平的影响。结果：去内皮组CPP、LVEDP、LDH、MDA及心律失常严重指数（ASI）均显著低于冠脉内皮保留组（P＜0．05或P＜0．01），而Na －K ATPase显著高于冠脉内应保留组（P＜0．05）。提示：去冠脉内皮细胞可减轻OFR对心肌的损伤，冠脉内皮至少部分介导OFR对心肌的损伤，亦说明冠脉内皮细胞在心肌损伤中所发挥的重要作用。     

Effects of Arecoline on Calcium Channel Currents and Caffeine—induced Calcium Release in Isolated Single Ventricular Myocyte of Guinea Pig

Summary The effects of Arecoline (Are) on calcium mobilization were investigated. In isolated single ventricular myocyte of guinea pig, patch clamp whole cell recording techniques were used to record the current of L-type calcium channel and cytosolic Ca²⁺ level (Ca²⁺i) labeled with fluorescence probe Fluo-3/AM was measured under a laser scanning confocal microscope. Results revealed that Are (3–100 μmol/L) could inhibit L-type calcium current in a concentration-dependent manner and the value of IC₅₀ was 33.73 μmol/L (n=5). In the absence of extracellular calcium, the resting levels of [Ca²⁺]i was not affected by Are (n=6,P>0.05), but pretreatment with Are (30 μmol/L) could significantly inhibit the [Ca²⁺]i elevation induced by caffeine (10 mmol/L,n=6,P<0.01). It was concluded that Are could inhibit not only calcium influx through L-type calcium channel but also calcium release from sarcoplasmic reticulum. This project was supported by a grant from Natural Sciences Foundation of China (No. 39670661).     

马来酸罗格列酮对大鼠脑缺血及再灌注后炎症的影响

 目的探讨马来酸罗格列酮对脑缺血后炎症反应影响,以评价马来酸罗格列酮对脑缺血损伤的保护作用。方法大鼠大脑中动脉线栓法建立局灶性脑缺血模型,缺血即刻及缺血2h后经插入胃管分别灌入马来酸罗格列酮0.5,2,4mg·kg^-1,测定缺血24h后,大鼠脑肿胀情况,脑组织髓过氧化物酶(MPO)活性,以及缺血2h并再灌注22h后脑组织髓过氧化物酶(MPO)活性和IL-6mRNA表达的影响。结果马来酸罗格列酮0.5mg·kg^-1对脑肿胀改变无明显影响(P>0.05),2,4mg·kg^-1实验组脑肿胀可见明显减轻(P<0.05),但二者之间无显著差异;各种不同剂量的马来酸罗格列酮可明显抑制缺血及再灌注大鼠的MPO水平(P<0.05,P<0.01),且抑制程度呈剂量相关;马来酸罗格列酮0.5,2mg·kg^-1可一定程度降低缺血再灌注脑组织IL-6 mRNA表达的水平(P<0.05),两剂量组之间有显著差异。结论马来酸罗格列酮可有效抑制脑缺血和再灌注后脑损伤。