A study on the effects of endogenous nitric oxide on coronary blood flow, myocardial oxygen extraction and cardiac contractility

The purpose of the present study was to clarify how endogenous nitric oxide (NO) affects cardiac contractility and myocardial oxygen consumption (MVO2 ) in vivo. alpha-Chloralose-anesthetized dogs (n = 18) were instrumented to perform continuous and simultaneous measurements of coronary blood flow (C BF), anterior interventricular vein oxygen saturation (with the use of a fi beroptic catheter), aortic pressure, left ventricular pressure, and left ve ntricular volume. CBF, myocardial oxygen extraction (O-2-extract), MVO2, th e relationship between CBF and O-2-extract during direct vasodilation induc ed by intracoronary papaverine (0.1, 0.2, 0.4 mg/kg), and cardiac contracti lity (E-max) were examined at control, after intracoronary infusion of N-G- monomethyl-L arginine (L-NMMA, 2 mg/kg) and after antagonization of NO by L -arginine (20 mg/kg). L-NMMA decreased CBF from 62.0 +/- 1.7 to 59.7 +/- 2. 4 (mL/min/100 g, P < 0.05) and increased O-2-extract from 68.2 +/- 1.7 to 7 9.0 +/- 1.7% (P < 0.05). E-max was increased after L-NMMA from 3.2 +/- 0.2 to 3.7 +/- 0.1 (mmHg/mL/100 g, P < 0.05). These effects of L-NMMA were anta gonized by L-arginine (P < 0.05 vs. after L-NMMA, P = NS vs, before L-NMMA) . L-NMMA shifted CBF and O-2-extract relationship determined by papaverine injection upward and L-arginine antagonized it to its baseline level. Endog enous NO reduces cardiac contractility and decreases MVO2, while increasing CBF. (C) Elsevier, Paris.