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心肌儿茶酚胺在缺血和再灌注期间对细胞电生理及心律失常的有害影响。

The deleterious effects of myocardial catecholamines on cellular electrophysiology and arrhythmias during ischaemia and reperfusion.

作者信息

Penny W J

出版信息

Eur Heart J. 1984 Dec;5(12):960-73. doi: 10.1093/oxfordjournals.eurheartj.a061616.

DOI:10.1093/oxfordjournals.eurheartj.a061616
PMID:6442888
Abstract

Action potentials and ECGs were recorded from Langendorff perfused guinea pig hearts during ischaemia and reperfusion. Arrhythmias were significantly more frequent during low flow (10% of control) than zero flow ischaemia and were most frequent during reperfusion following 30 minute ischaemia. Arrhythmias during low flow ischaemia were preceded by spontaneous recovery in action potential amplitude and Vmax and marked shortening of refractory period which did not occur during zero flow ischaemia. Reperfusion VF was always preceded by further shortening of the action potential. Myocardial catecholamine depletion, by pre-treatment with 6-hydroxydopamine significantly reduced the incidence of arrhythmias during ischaemia and reperfusion. Catecholamine depletion blunted the ischaemia-induced reduction in action potential amplitude and Vmax, prevented any spontaneous recovery and abolished reperfusion induced shortening of action potential duration. Methoxamine given to catecholamine-depleted hearts, having only minor effects during normal perfusion, significantly reversed the anti-arrhythmic and electrophysiological effects of catecholamine depletion during ischaemia and reperfusion. Phentolamine and propranolol in anti-arrhythmic concentrations, profoundly modified the electrophysiological effects of ischaemia and reperfusion. These results suggest that release of endogenous myocardial catecholamines contributes through alpha and beta-adrenoceptor stimulation to the electrophysiological changes and arrhythmias during myocardial ischaemia and reperfusion.

摘要

在缺血和再灌注期间,从Langendorff灌注的豚鼠心脏记录动作电位和心电图。低流量(对照的10%)缺血期间心律失常的发生率明显高于零流量缺血,且在30分钟缺血后的再灌注期间最为频繁。低流量缺血期间的心律失常之前,动作电位幅度和Vmax会自发恢复,不应期明显缩短,而零流量缺血期间则不会出现这种情况。再灌注室颤之前,动作电位总是会进一步缩短。通过用6-羟基多巴胺预处理使心肌儿茶酚胺耗竭,可显著降低缺血和再灌注期间心律失常的发生率。儿茶酚胺耗竭减弱了缺血诱导的动作电位幅度和Vmax降低,阻止了任何自发恢复,并消除了再灌注诱导的动作电位持续时间缩短。给予儿茶酚胺耗竭心脏的甲氧明,在正常灌注期间只有轻微作用,在缺血和再灌注期间可显著逆转儿茶酚胺耗竭的抗心律失常和电生理作用。抗心律失常浓度的酚妥拉明和普萘洛尔可深刻改变缺血和再灌注的电生理作用。这些结果表明,内源性心肌儿茶酚胺的释放通过α和β肾上腺素能受体刺激,促成了心肌缺血和再灌注期间的电生理变化和心律失常。

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