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J Thorac Cardiovasc Surg 2000;119:94-100
© 2000 Mosby, Inc.

SURGERY FOR ACQUIRED CARDIOVASCULAR DISEASE

COMPARATIVE STUDY ON CALCIUM CHANNEL ANTAGONISTS IN THE HUMAN RADIAL ARTERY: CLINICAL IMPLICATIONS

From the Cardiovascular Research Laboratory and Division of Cardiothoracic Surgery, Department of Surgery, University of Hong Kong, Grantham Hospital, Aberdeen, Hong Kong, and Cardiovascular Research Laboratory, Starr Academic Center for Cardiac Surgery, St Vincent Hospital, Portland, Ore.

Supported by Hong Kong Research Grants Council (HKU7280/97M and HKU7246/99M), Committee of Research and Conference Grant (337/048/0018, 335/048/0079), and St Vincent Medical Foundation, Portland, Ore.

Address for reprints: Professor Guo-Wei He, MD, PhD, Chair of Cardiothoracic Surgery, University of Hong Kong, Grantham Hospital, 125 Wong Chuk Hang Rd, Aberdeen, Hong Kong (E-mail: gwhe{at}hkucc.hku.hk).

Objectives: The radial artery is spastic, and calcium channel antagonists have been used clinically in the radial artery for their antispastic effects. To choose a proper calcium channel antagonist for such a purpose, we compared the in vitro antispastic effects of 4 clinically used calcium channel antagonists (nicardipine, nifedipine, verapamil, and diltiazem) in the human radial artery.
Methods: Radial artery segments taken from patients undergoing coronary bypass operations were studied in the organ bath. The relaxation by the calcium channel antagonists was compared in the potassium-precontracted (25 mmol/L) radial artery. The inhibitory effect of the calcium channel antagonists at the clinically relevant plasma concentration and a higher concentration was also studied for the calcium channel antagonists.
Results: All calcium channel antagonists induced a full relaxation (97.8%-100%, n = 5-7 for each), with higher sensitivity (P = .005, analysis of variance [ANOVA] among the calcium channel antagonists for the effective concentration of the constrictor [or dilator] agent that caused 50% of maximal contraction [or relaxation]) to nifedipine (–7.37 ± 0.20 log₁₀ M) than nicardipine (–6.43 ± 0.39 log₁₀ M, P = .1), verapamil (–6.08 ± 0.13 log₁₀ M, P = .03), and diltiazem (–5.87 ± 0.07 log₁₀ M, P = .01). Pretreatment with the plasma concentration of the calcium channel antagonists (60 nmol/L for diltiazem and 20 nmol/L for the others) inhibited the potassium-induced contraction (n = 6 for each) by nicardipine (from 138.6% ± 5.8% to 101.4% ± 7.6%, P = .001) and nifedipine (to 87.7% ± 6.8%, P = .0003) but not by verapamil (to 140.3% ± 15.2%, P = .9) or diltiazem (to 132.8% ± 7.3%, P = .8), although at higher contractions (–4.5 log₁₀ M) all 4 calcium channel antagonists abolished the contraction.
Conclusions: Although all calcium channel antagonists have antispastic effects in the radial artery, the vessel has different sensitivities to them. Dihydropyridine derivatives may be the most potent calcium channel antiagonists and therefore are recommended for the clinical use for this purpose.

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