Manukhina E B, Lapshin A V, Meerson F Z
Fiziol Zh (1978). 1991 May-Jun;37(3):98-105.
Acute stress concomitant to the experimental myocardial infarction has induced endothelial hyperactivation of the rat aorta exhibited in an increase of inhibition of norepinephrine-induced contractions of vascular smooth muscle, enhanced endothelium-dependent relaxation correlating with a fall of systemic blood pressure. Preliminary adaptation of rats to intermittent hypobaric hypoxia greatly prevented the stress-induced endothelial hyperactivation and beneficially affected the postinfarction time course of blood pressure.
实验性心肌梗死伴随的急性应激已诱导大鼠主动脉内皮细胞过度激活,表现为去甲肾上腺素诱导的血管平滑肌收缩抑制增加、内皮依赖性舒张增强,这与全身血压下降相关。大鼠对间歇性低压缺氧的初步适应极大地预防了应激诱导的内皮细胞过度激活,并对心肌梗死后的血压变化过程产生有益影响。