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肾上腺素诱导心肌缺血的机制:与运动诱导缺血的比较。

Mechanisms of myocardial ischemia induced by epinephrine: comparison with exercise-induced ischemia.

作者信息

Sung B H, Wilson M F, Robinson C, Thadani U, Lovallo W R

机构信息

College of Pharmacy, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City.

出版信息

Psychosom Med. 1988 Jul-Aug;50(4):381-93. doi: 10.1097/00006842-198807000-00006.

Abstract

The role of epinephrine in eliciting myocardial ischemia was examined in patients with coronary artery disease. Objective signs of ischemia and factors increasing myocardial oxygen consumption were compared during epinephrine infusion and supine bicycle exercise. Both epinephrine and exercise produced myocardial ischemia as evidenced by ST segment depression and angina. However, the mechanisms of myocardial ischemia induced by epinephrine were significantly different from those of exercise. Exercise-induced myocardial ischemia was marked predominantly by increased heart rate and rate-pressure product with a minor contribution of end-diastolic volume, while epinephrine-induced ischemia was characterized by a marked increase in contractility and a less pronounced increase in heart rate and rate-pressure product. These findings indicate that ischemia produced by epinephrine, as may occur during states of emotional distress, has a mechanism distinct from that due to physical exertion.

摘要

在冠心病患者中研究了肾上腺素引发心肌缺血的作用。在输注肾上腺素和仰卧位自行车运动期间,比较了缺血的客观体征以及增加心肌耗氧量的因素。肾上腺素和运动均导致心肌缺血,表现为ST段压低和心绞痛。然而,肾上腺素诱发心肌缺血的机制与运动诱发的机制显著不同。运动诱发的心肌缺血主要表现为心率和心率-血压乘积增加,舒张末期容积的作用较小,而肾上腺素诱发的缺血特征为收缩力显著增加,心率和心率-血压乘积增加不明显。这些发现表明,在情绪困扰状态下可能发生的由肾上腺素产生的缺血,其机制与体力活动所致的机制不同。

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