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

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 CaCl in dogs. Methods: The left anterior descending coronary 2 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 21 (MVO) and oxygen extraction (EO) were calculated. Responses were assessed during i.c. infusions of CaCl (5, 10, 15 mg min) 2 2 2 G 21 before and after administration of the NO synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME; 300 mg min for 15 min, i.c.). Results: Before L-NAME, CaCl caused dose-dependent, proportional increases in SS and MVO. Although CBF also increased, these 2 2 responses were less than proportional to those in MVO , and thus EO increased. L-NAME did not alter the cardiac effects of CaCl. 2 2 2 Conclusions: (1) CaCl had direct inotropic and coronary vasoconstricting effects. (2) The vasoconstricting effect impaired coupling of 2 CBF to the augmented metabolic demands by local vasodilating mechanisms. (3) EDNO did not modulate the increases in CBF, MVO , 2 or SS during administration of CaCl .