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Ann Thorac Surg 2002;73:516-522
© 2002 The Society of Thoracic Surgeons

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Original article: cardiovascular

Interaction between vasodilators and vasopressin in internal mammary artery and clinical significance

^a Cardiovascular Research, Starr Academic Center, Providence Heart Institute, Department of Surgery, Oregon Health Sciences University, Portland, Oregon, USA
^b Division of Cardiothoracic Surgery, Department of Surgery, The Chinese University of Hong Kong, Hong Kong SAR, China

Accepted for publication September 19, 2001.

* Address reprint requests to Dr He, Department of Surgery, The Chinese University of Hong Kong, Block B, 5A, Prince of Wales Hospital, Shatin, N.T., Hong Kong SAR, China
e-mail: gwhe{at}cuhk.edu.hk

Background. Arginine vasopressin (AVP) has recently been demonstrated as an alternative in the treatment of severe refractory vasodilatation in coronary artery bypass grafting. However, AVP may be a spasmogen for graft spasm. We compared the in vitro antispastic effect among calcium-channel antagonists (nifedipine, diltiazem, and verapamil), nitroglycerin, and the highly selective AVP (V1) receptor antagonist [1-deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin.

Methods. Human internal mammary artery segments (n = 218) were studied in organ baths. The inhibitory effects of the above vasodilators on AVP-mediated contraction were studied in two ways: relaxation with AVP precontraction and depression of the AVP-induced contraction after pretreatment with vasodilators.

Results. All three calcium-channel antagonists caused limited relaxation (18.3% ± 5.4% for nifedipine, n = 11; 22.2% ± 3.8% for verapamil, n = 10; and 26.2% ± 7.5% for diltiazem, n = 9). The plasma concentration of calcium-channel antagonists had no significant depression effect on the AVP-induced contraction. In contrast, [1-deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin caused full (100%, n = 11) and nitroglycerin caused nearly full (93% ± 3%, n = 10) relaxation. Pretreatment with [1-deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin (10^-8, 10^-7, or 10^-6 mol/L, respectively) significantly increased the effective concentration for 50% of the AVP-induced contraction (10^-8.6 ± 10^0.1 mol/L, p = 0.009; 10^-7.8 ± 10^0.07 mol/L, p = 0.000; or 10^-6.9 ± 10^0.11 mol/L, p = 0.000 versus the control, 10^-9.24 ± 10^0.16 mol/L). However, nitroglycerin only slightly depressed the AVP-induced contraction.

Conclusions. [1-Deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin may provide specific antispastic effect in either prophylaxis or treatment of the AVP-related vasospasm in the internal mammary artery. Nitroglycerin may be effective in treatment but has little effect on prophylaxis. Use of calcium-channel antagonists may have little benefit in AVP-related vasospasm.

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