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J Thorac Cardiovasc Surg 1995;109:99-105
© 1995 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

Endothelium-dependent contraction of canine coronary artery is enhanced by crystalloid cardioplegic solution

Taipei, Taiwan, Republic of China

Supported in part by grant NSC 83-0412 B-182-018 from the National Science Council, Executive Yuan, Taiwan, Republic of China, and by the grant 355 from the Chang Gung Memorial Hospital, Chang Gung Medical College, Taipei, Taiwan, Republic of China.

Received for publication Jan. 6, 1994. Accepted for publication May 30, 1994. Address for reprints: Pyng Jing Lin, MD, Division of Thoracic and Cardiovascular Surgery, Chang Gung Memorial Hospital, 199, Tun-Hwa North Rd., Taipei, Taiwan, Republic of China.

Abstract

Experiments were designed to determine whether hyperkalemic crystalloid cardioplegic solution enhances endothelium-dependent contraction of coronary arteries. Segments of canine coronary arteries (n = 8 in each group) were preserved in cold (4° C) crystalloid cardioplegic solution (group 1) and physiologic solution (group 2) for 60 minutes. Segments of preserved and control (group 3) coronary arteries with or without endothelium were suspended in organ chambers to measure isometric force. Perfusate hypoxia (oxygen tension 35 ± 5 mm Hg) caused endothelium-dependent contraction in the arteries of all three groups. However, vascular segments with endothelium of group 1 exhibited hypoxic contraction (68.5% ± 15.3% of the initial tension contracted by prostaglandin F ₂2 x 10 ^-6 mol/L, p < 0.05) that was significantly greater than contraction of the group 2 and group 3 segments with endothelium (26.6% ± 5.6% and 20.6 ± 4.4%). The hypoxic contraction in arteries of group 1 could be attenuated by N^G -monomethyl-L-arginine, the blocker of endothelial cell synthesis of the nitric oxide from L-arginine. The action of N^G -monomethyl-L-arginine could be reversed by L-arginine but not D-arginine. Thus after preservation with cardioplegic solution, augmented endothelium-dependent contraction, occurs by L-arginine-dependent pathway, would favor coronary vasospasm after cardiac operation. (J THORAC CARDIOVASC SURG 1995;109:99-105)

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