Release of Endogenous Catecholamines in the Ischemic Myocardium of the Rat: Part A Locally Mediated Release
Release of Endogenous Catecholamines in the Ischemic Myocardium of the Rat: Part A Locally Mediated Release
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大鼠缺血心肌内源性儿茶酚胺的释放：A 部分局部介导的释放
DOI：
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发表时间：
1984
影响因子：
20.1
通讯作者：
Wolfgang Kiibler
中科院分区：
文献类型：
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作者：
A. Schomig;A. Dart;R. Dietz;E. Mayer;Wolfgang Kiibler
在大鼠心脏处于不同时期的完全缺血状态下，研究了内源性儿茶酚胺在缺血心肌细胞外间隙内的积聚。儿茶酚胺和脱氨代谢物的测定采用放射酶法或高压液相色谱仪。小于10分钟的缺血期与儿茶酚胺或代谢物溢出增加无关。较长时间的缺血伴随去甲肾上腺素及其脱氨代谢物3，4-二羟基苯甘醇的溢出。随着前一次缺血时间的延长(10分钟：2.5±0.6，20分钟：209.8±17.2，60分钟：1270.5±148.1 pmol去甲肾上腺素/克心脏)，这种溢出增加。去甲肾上腺素浓度在再灌流的第一分钟内最高，这表明在再灌流期间检测到的去甲肾上腺素在缺血时被释放到心肌细胞外间隙，随后被洗脱。细胞外钙浓度变化和神经元摄取阻滞剂的实验表明，儿茶酚胺释放的不同机制在缺血过程中起作用。钙非依赖性载体介导的去甲肾上腺素从神经末梢流出是非常重要的，使用的载体与正常情况下负责将去甲肾上腺素从突触间隙输送到神经元静脉曲张的载体相同。因此，在10到40分钟的缺血期后，不同的Up-1阻滞剂可以减少去甲肾上腺素的溢出。较长时间的缺血后去甲肾上腺素的溢出不受摄取阻滞剂的影响，此时额外的去甲肾上腺素释放可能是细胞膜溶解的结果。肾上腺素和多巴胺的溢出程度较小(不到相应去甲肾上腺素溢出的5%)，并且只有在缺血超过15分钟后才会出现。
The accumulation of endogenous catecholamines within the extracellular space of the ischemic myocardium has been studied in the isolated perfused (Langendorff) heart of the rat subjected to various periods of complete ischemia, with subsequent collection of the reperfusate. Catecholamines and deaminated metabolites were measured by radioenzymatic methods, or high pressure liquid chromatography. Ischemic periods of less than 10 minutes are not associated with an increased overflow of catecholamines or metabolites. Longer periods of ischemia are accompanied by the overflow of noradrenaline and its deaminated metabolite 3,4-dihydroxyphenylgly-col. This overflow increases with lengthening of the preceding ischemic period (10 minutes: 2.5 ± 0.6, 20 minutes: 209.8 ± 17.2, 60 minutes: 1270.5 ± 148.1 pmol noradrenaline/g heart). Noradrenaline concentration is highest during the first minute of reperfusion, suggesting that the noradrenaline detected during reperfusion is released into the extracellular space of the myocardium during ischemia and is subsequently eluted. Experiments with variation of extracellular calcium concentration and with neuronal uptake (uptakei) blocking agents suggest that different mechanisms of catecholamine release are acting during the course of ischemia. A calcium-independent carrier-mediated efflux of noradrenaline from the nerve terminals is of major importance, using the same carrier as is normally responsible for transporting noradrenaline from the synaptic clefts into the neuronal varicosities. Thus, various uptake1-blocking agents diminish the noradrenaline overflow following ischemic periods of between 10 and 40 minutes. The noradrenaline overflow following longer periods of ischemia is unaffected by uptake]-blocking agents, and additional noradrenaline release at this time is probably consequent upon dissolution of cell membranes. Overflow of adrenaline and dopamine occurs to a minor degree (less than 5% of the corresponding noradrenaline overflow), and only after ischemic periods of more than 15 minutes.