Mosinger B, Stejskal J, Tutterová M, Vavrínková H
Eur J Cardiol. 1978 Jan;6(5):389-402.
Isolated rat hearts were perfused using a retrograde technique under constant pressure head or constant coronary flow. The addition of 1-epinephrine or 1-norepinephrine (1 microgram/ml) to the perfusion medium for 1 h caused visible and irreversible morphological changes which usually became apparent after 4 h of perfusion in the form of small, pale, opaque spots or streaks gradually enlarging on the surface or on the cross-section area of the myocardium. Light- and electron-microscopic examination showed a disintegration process analogous to that of myocardial infarction but without the infiltration with blood elements. The structural changes were preceded by an increased release of lactate dehydrogenase into the effluent, the most characteristic metabolic change accompanying myocardial injury. Nevertheless, the underlying mechanism of the cardiotoxic action of catecholamines remains to be clarified; several factors under consideration could be eliminated: hyperlipidemia, trombogenic process, acidity due to enhanced production of lactate, reduced total coronary inflow rate and toxicity of oxidation products of catecholamines.
采用逆行灌注技术,在恒压头或恒定冠脉流量条件下对离体大鼠心脏进行灌注。向灌注液中加入1-肾上腺素或1-去甲肾上腺素(1微克/毫升),持续1小时,会导致明显且不可逆的形态学改变,这种改变通常在灌注4小时后变得明显,表现为心肌表面或横截面上出现小的、苍白的、不透明的斑点或条纹,并逐渐扩大。光镜和电镜检查显示出类似于心肌梗死的崩解过程,但没有血液成分的浸润。在结构变化之前,乳酸脱氢酶向流出液中的释放增加,这是心肌损伤伴随的最典型代谢变化。然而,儿茶酚胺心脏毒性作用的潜在机制仍有待阐明;一些考虑因素可以排除:高脂血症、血栓形成过程、乳酸生成增加导致的酸度、总冠脉流入速率降低以及儿茶酚胺氧化产物的毒性。