老年男性心肌缺血患者心率变异分析（附67例报告）

采用正常搏动ＲＲ间期的标准差（ＳＤ）及心率变异指数（ＨＲＶ ｉｎｄｅｘ）作为指标，分析６７例老年男性心肌缺血患者的心率变异，并与正常老年男性组及正常青壮年男性组进行了对比，发现前组的ＲＲ间期ＳＤ、ＨＲＶｉｎｄｅｘ均明显低于后两组，其结果有显著性差异（Ｐ均〈０．０１）。提示心肌缺血可破坏交感与迷走神经的均衡性，造成心率变异降低。     

Striatal cells containing the Ca2+-binding protein calretinin (protein 10) in ischemia-induced neuronal injury

The present study concerns the vulnerability of striatal interneurons immunopositive for the Ca²⁺-binding protein calretinin to ischemic neuronal injury. An immunohistochemical study was carried out on the striata of rats which had undergone transient middle cerebral artery occlusion. Two weeks after the ischemia, there was a marked reduction in the number of calretinin-positive neurons in the ipsilateral ischemic lesion, although the striatal interneurons positive for parvalbumin, which are a neuronal population distinct from the calretinin-immunoreactive cells in the striatum, were spared in the insulted areas. The present data indicate that the striatal calretinin-positive neurons are less resistant to transient ischemia, suggesting that there may exist vulnerability differences among the striatal interneurons in ischemia-induced neuronal injury.     

NO对兔局灶脑缺血脑水肿和脑梗塞灶的影响

本文在兔MCAO局灶脑缺血模型基础上,利用外源性一氧化氮(NO)前体物质L-精氨酸和NOS抑制剂L-NNA研究NO对脑缺血后脑水肿和脑梗塞的影响。NZW兔42只随机分为7组,每组6只,计对照组、假手术组、MCAO组、MCAO+NS组、MCAO+L-Arg组、MCAO+D-Arg组及MCAO+L-Arg+L-NNA组。结果提示:与单纯MCAO组比较,L-Arg组的脑组织H_2O、Na~+、Ca~(2+)含量明显下降(P<0.01),脑梗塞灶亦明显缩小(P<0.01)。从而显示L-Arg系通过产生NO促使血管舒张而减轻脑水肿和缩小梗塞灶,为临床改进脑缺血的治疗提供依据。     

Ascorbic acid prevents ischemia-reperfusion injury in the rat small intestine

Ischemia-reperfusion injury by free radicals and lipid peroxides is observed in various organs. Ascorbic acid (AsA) or glutathione (GSH) in various doses (AsA:2, 0.5, 0.1 mmol/kg, GSH:2 mmol/kg) was intraperitoneally administered to male Wistar rats. The entire small intestines were resected just before ischemia, after ischemia, and after 20 min of reperfusion (n = 7–10 at each time point). At each time point, the specimens were subjected to assays of lipid peroxides, GSH, and glutaminase activity of the tissues; they were also examined histologically. In the AsA group, the production of lipid peroxides after reperfusion was significantly suppressed in a dose-dependent manner, and the ratio of oxidized GSH to total GSH was also significantly low. Tissue glutaminase activity decreased to a lesser extent, and the degree of injury was apparently less marked in the AsA group. This study indicates that AsA acts as an antioxidant against peroxidative tissue injury, possibly by scavenging radicals, preserving reduced GSH, and reducing the peroxidative reaction. Received: 21 June 1996 Received after revision: 8 October 1996 Accepted: 12 November 1996     

间断缺血心停搏在冠脉搭桥术中的应用

１９９２～１９９３年间为１８０例冠脉病变的病人施行冠脉搭桥术，全部病人均采用核甙抑制剂利多氟嗪预处理和低温（２８℃）间断缺血心停搏进行术中心肌保护。平均每例病人作冠状动脉端吻合３～４个，每个吻合口用９分钟，主动脉阻断累加时间约２５分钟，体外循环时间９０分钟，术后医院死亡率１．６％（３／１８０），无术后心梗发生。作者认为，冠脉搭桥术的术中心肌保护可采用核甙抑制剂和间断缺血心停搏方法，而不用心肌停搏液。     

温缺血时间与同种心脏瓣膜细胞活性的关系

以１０具脑外伤死亡的健康男性的心脏的６０个同种主动脉、肺动脉瓣叶分为６组进行实验。经不同的温缺血时间灭菌并经过３个月的液氮深低温保存后，通过流式细胞计数测定细胞活性，同时行组织块贴壁培养及电镜观察。结果表明：温缺血时间在１２小时以内，细胞活性为９３．４９±２．３５％，较对照组无明显下降。灭菌２４小时，细胞活性为８９．８２±３．５２％，较对照组明显下降，Ｐ＜０．０１，并且可见形态上改变；冷冻后细胞活性进一步下降，但下降幅度减低，冻存３年后活细胞仍占８０％。结论为：温缺血时间对细胞活性有影响，时间延长与活性的下降成正相关。因此温缺血时间应控制在１２小时以内。     

常温体外循环下采用缺血预调行心肌保护的研究

为了探讨常温体外循环下采用缺血预调行心肌保护的研究,通过建立犬的常温体外循环全心缺血预调模型,旨在探讨心内直视手术缺血预调保护心肌的可能性。预调组采用升主动脉阻断5分钟,放开10分钟,反复三次的方式预调心脏;对照纽简单并行循环45分钟,而后两组均接受30分钟缺血和60分钟再灌注。结果显示,预调组室颤发生率低(16.7 VS 83.3％P=0.04),无再灌注心律失常(0 VS66.7％P=0.03),心肌ATP消耗减慢(4.69 1.050 VS 2.35±0.86μmol/g wet wt P<0.01),乳酸积累减少(4.49±0.86 VS 9.80 5.53mg/g wet wtP<0.05),心肌细胞超微结构损伤轻。结论:常温体外循环下应用缺血预调保护犬的心肌是可行而有效的。     

Quantitative analysis of the tomographic technetium-99m MIBI (99mTc-MIBI) myocardial bullseye display: Application to diagnosis of coronary artery disease

Summary In this study, the^99mTc-MIBI myocardial bullseye display of 31 healthy persons and 34 patients with myocardial ischemia and 17 patients with myocardial infarction were analyzed quantitatively, and compared with the results of myocardial tomography analysis and qualitative bullseye analysis. The sensitivities of the three methods were 88.2%, 91.2% and 94.1% respectively (P>0.05), and the specificities were 93.5%, 83, 9% and 83.9% respectively (P<0.05). On the other hand, the quantitative analysis obviously outperformed the other two methods in the detection of ischemic segments of myocardhum near infarction zone (P<0.01). The quantitative analysis of^99mTc-MLBI myocardial bullseye (quantitative bullseye) was an objective, specific and sensitive method for diagnosis of coronary artery disease.     

REPERFUSION FOLLOWING MYOCARDIAL ISCHAEMIA ENHANCES INOSITOL PHOSPHATE RELEASE IN THE ISOLATED PERFUSED RAT HEART

1. Global myocariial ischaemia (MI) for periods greater tan 5 min caused an inhibition of phosphatidylinositol specific phospholipase C (PtdIns-PLC) activity. 2. Two min reperfusion following a 20 min MI period, a time point associated with reperfusion-induced arrhythmias, resulted in an activation of PtdIns-PLC activity, dependent on endogenous noradrenaline and mediated via al-adrenoceptors. 3. This 2 min reperfusion response, in contrast to healthy myocardium, resulted in: (i) enhanced PtdIns-PLC activity; (ii) increased sensitivity to endogenous noradrenaline; (iii) rapid increases in inositol(1,4,5)trisphosphate (Ins(1,4,5)P3); and (iv) PLC hydrolysis primarily of PtdIns(4,5)P₂, such that the majority of InsP isomers derive from Ins(1,4,5)P₃. 4. Together, these data suggest a functional role for Ins(1,4,5)P3 under postischaemic reperfusion conditions, and provide a possible link between al-adrenoceptor stimulation of the PtdIns turnover pathway and reperfusion injury.