Meerson F Z, Lapshin A V, Manukhina E B
Fiziol Zh SSSR Im I M Sechenova. 1991 Jul;77(7):48-56.
The stress concomitant with experimental myocardial infarction resulted in endothelial hyperactivation of the isolated rat aorta. The hyperactivation was manifested in potentiated inhibition of norepinephrine-induced contractions of vascular smooth muscle, increased endothelium-dependent relaxation and respective drop of systemic blood pressure. Preliminary treatment of animals with synthetic antioxidant ionol prevented the stress-induced endothelial hyperactivation and beneficially affected the postinfarction time course of blood pressure. The data suggest that the endothelial hyperactivation observed in acute myocardial infarction is induced by stress-induced activation of free-radical oxidation which results in a hyperproduction of endothelium-derived relaxing factor (nitric oxide).
实验性心肌梗死伴随的应激导致离体大鼠主动脉内皮细胞过度激活。这种过度激活表现为去甲肾上腺素诱导的血管平滑肌收缩受到增强抑制、内皮依赖性舒张增加以及体循环血压相应下降。用合成抗氧化剂离子醇对动物进行预处理可预防应激诱导的内皮细胞过度激活，并对梗死后血压的病程产生有益影响。数据表明，急性心肌梗死中观察到的内皮细胞过度激活是由应激诱导的自由基氧化激活所致，这导致内皮衍生舒张因子（一氧化氮）过度产生。
