Hough F S, Gevers W
S Afr Med J. 1975 Mar 29;49(14):538-43.
Isolated rat hearts perfused at suboptimal pressures have been studied as a model for generalised myocardial ischaemia. Glycogen phosphorylase a and hormone-sensitive triglyceridase activities, measured as markers for endogenous catecholamine release, were significantly increased at low perfusion pressures. Pharmacological blockage of noradrenaline re-uptake accentuated these effects, and depletion of catecholamine reserves eliminated them. This phenomenon may be important in the pathophysiology of cardiac ischaemia and its serious complications.
以低于最佳压力灌注的离体大鼠心脏已作为全身性心肌缺血的模型进行了研究。作为内源性儿茶酚胺释放标志物测定的糖原磷酸化酶a和激素敏感性甘油三酯酶活性在低灌注压力下显著增加。去甲肾上腺素再摄取的药理学阻断加剧了这些作用，而儿茶酚胺储备的耗竭则消除了这些作用。这种现象可能在心脏缺血及其严重并发症的病理生理学中具有重要意义。
