Nitric oxide does not modulate the increases in blood flow, O-2 consumption, or contractility during CaCl2 administration in canine hearts

Citation
Gj. Crystal et Xp. Zhou, Nitric oxide does not modulate the increases in blood flow, O-2 consumption, or contractility during CaCl2 administration in canine hearts, CARDIO RES, 42(1), 1999, pp. 232-239
Citations number
43
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR RESEARCH
ISSN journal
00086363 → ACNP
Volume
42
Issue
1
Year of publication
1999
Pages
232 - 239
Database
ISI
SICI code
0008-6363(199904)42:1<232:NODNMT>2.0.ZU;2-G
Abstract
Objective: Endothelium-derived nitric oxide (EDNO) has been shown to have v ascular, metabolic, and contractile effects in the heart. We evaluated thes e effects during intracoronary (i.c.) administration of CaCl2 in dogs. Meth ods: The left anterior descending coronary artery of nine anesthetized, ope n-chest dogs was perfused at controlled pressure (80 mm Hg) with arterial b lood. Coronary blood flow (CBF) was measured with a Doppler transducer and segmental shortening (SS) with ultrasonic crystals. Myocardial oxygen consu mption (MVO2) and oxygen extraction (EO2) were calculated. Responses were a ssessed during i.c. infusions of CaCl2 (5, 10, 15 mg min(-1)) before and af ter administration of the NO synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME; 300 mu g min(-1) for 15 min, i.c.). Results: Before L-NAME, CaCl2 caused dose-dependent, proportional increases in SS and MVO2. Althou gh 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 vasocons tricting effects. (2) The vasoconstricting effect impaired coupling of CBF to the augmented metabolic demands by local vasodilating mechanisms. (3) ED NO did not modulate the increases in CBF, MVO2, or SS during administration of CaCl2. (C) 1999 Elsevier Science B.V. All rights reserved.