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Ann Thorac Surg 2000;70:627-632
© 2000 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Effects of angiotensin-converting enzyme inhibitor during warm blood cardioplegia

^a Department of Surgery, Kurume University, Fukuoka, Japan

Address reprint requests to Dr Hayashida, Department of Surgery, Kurume University, 67 Asahi-machi, Kurume, Fukuoka 830-0011, Japan
e-mail: nobuhiko{at}med.kurume-u.ac.jp

Background. Effects of captopril, an angiotensin-converting enzyme inhibitor, during warm blood cardioplegia were assessed in the blood-perfused, isolated rat heart.

Methods. The isolated hearts were arrested for 60 minutes with warm blood cardioplegia given at 20-minute intervals and were reperfused for 60 minutes. The control group ( ) received standard cardioplegia and the captopril group ( ) received cardioplegia supplemented with captopril (2 mmol/L). Cardiac function, myocardial metabolism, and cardiac release of circulating adhesion molecules were assessed before and after cardioplegic arrest.

Results. Left ventricular end-diastolic pressure and -dp/dt were significantly (p < 0.05) lower and coronary blood flow was significantly (p < 0.05) greater in the captopril group than the control group during reperfusion. The captopril group resulted in significantly (p < 0.05) less cardiac release of lactate, thiobarbituric acid reactive substances during reperfusion. Cardiac release of intercellular adhesion molecule-1 was significantly (p < 0.05) less in the captopril group at 60 minutes of reperfusion.

Conclusions. The results suggest that supplementation of captopril during warm blood cardioplegia provides superior myocardial protection by suppressing lipid peroxidation and leukocyte–endothelial cell interaction during reperfusion.

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