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Cardiovascular Research 1999 42(1):232-239; doi:10.1016/S0008-6363(98)00325-3
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Nitric oxide does not modulate the increases in blood flow, O2 consumption, or contractility during CaCl2 administration in canine hearts

George J Crystala,b,c,* and Xiping Zhoua,b

aDepartment of Anesthesiology, Illinois Masonic Medical Center, Chicago, IL 60657, USA
bDepartment of Anesthesiology, University of Illinois College of Medicine, Chicago, IL 60680, USA
cDepartment of Physiology and Biophysics, University of Illinois College of Medicine, Chicago, IL 60680, USA

* Corresponding author. Tel.: +1-773-296-5375; fax: +1-773-296-5362.

Objective: Endothelium-derived nitric oxide (EDNO) has been shown to have vascular, metabolic, and contractile effects in the heart. We evaluated these effects during intracoronary (i.c.) administration of CaCl2 in dogs. Methods: The left anterior descending coronary artery of nine anesthetized, open-chest dogs was perfused at controlled pressure (80 mm Hg) with arterial blood. Coronary blood flow (CBF) was measured with a Doppler transducer and segmental shortening (SS) with ultrasonic crystals. Myocardial oxygen consumption (MVO2) and oxygen extraction (EO2) were calculated. Responses were assessed during i.c. infusions of CaCl2 (5, 10, 15 mg min–1) before and after administration of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 300 µg min–1 for 15 min, i.c.). Results: Before L-NAME, CaCl2 caused dose-dependent, proportional increases in SS and MVO2. Although CBF also increased, these responses were less than proportional to those in MVO2, and thus EO2 increased. L-NAME did not alter the cardiac effects of CaCl2. Conclusions: (1) CaCl2 had direct inotropic and coronary vasoconstricting effects. (2) The vasoconstricting effect impaired coupling of CBF to the augmented metabolic demands by local vasodilating mechanisms. (3) EDNO did not modulate the increases in CBF, MVO2, or SS during administration of CaCl2.

KEYWORDS Coronary hemodynamics; Inotropic drugs; Cardiac performance; Dogs; NG-nitro-L-arginine methyl ester


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