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卡波铬引起的冠状动脉扩张对冠心病心肌代谢的影响。

Effect of carbocromen induced coronary vasodilatation on myocardial metabolism in coronary artery disease.

作者信息

Kjekshus J K, Simonsen S, Bøhmer T

出版信息

Clin Cardiol. 1978 Aug;1(2):74-9. doi: 10.1002/clc.4960010204.

Abstract

Myocardial metabolism was studied during coronary vasodilatation by carbocromen during atrial pacing in patients with coronary arteriosclerotic disease. Coronary sinus flow was measured by the continuous infusion thermodilution technique. Carbocromen increased myocardial flow by the same amount at rest and during pacing-induced tachycardia. The administration of carbocromen did not interfere with myocardial oxygen consumption, free fatty acid (FFA) uptake, pulmonary or systemic hemodynamics. Atrial pacing above the anginal threshold increased lactate and hypoxanthine excretion to the coronary sinus, but to a greater extent during carbocromen treatment. Thus, carbocromen is a specific coronary vasodilator acting independently of pacing induced vasodilatation. Metabolic data indicate a small but unfavourable effect on ischemic metabolism which might be due to a "coronary steal".

摘要

在患有冠状动脉粥样硬化疾病的患者中,通过心房起搏,研究了卡波铬在冠状动脉扩张期间的心肌代谢情况。采用连续输注热稀释技术测量冠状窦血流量。卡波铬在静息时和起搏诱发心动过速期间增加的心肌血流量相同。卡波铬的给药不影响心肌耗氧量、游离脂肪酸(FFA)摄取、肺或全身血流动力学。高于心绞痛阈值的心房起搏会增加乳酸和次黄嘌呤向冠状窦的排泄,但在卡波铬治疗期间增加的程度更大。因此,卡波铬是一种独立于起搏诱导的血管扩张作用的特异性冠状动脉扩张剂。代谢数据表明其对缺血代谢有轻微但不利的影响,这可能是由于“冠状动脉窃血”所致。

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