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ADENOSINE ON MYOCARDIAL OXYGEN CONSUMPTION
Author(s) -
GROSS G.J.,
HARDMAN H.F.,
WARLTIER D.C.
Publication year - 1976
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1976.tb07681.x
Subject(s) - coronary vasodilator , cardiology , medicine , chronotropic , adenosine , inotrope , perfusion , coronary perfusion pressure , blood pressure , blood flow , vasodilation , ventricular pressure , heart rate , coronary circulation , hemodynamics , anesthesia , cardiopulmonary resuscitation , resuscitation
1 A 3 min intracoronary infusion of adenosine (50 μg/min) produced a significant decrease in coronary artery perfusion pressure, left ventricular systolic pressure and myocardial O 2 consumption in the isolated supported heart preparation of the dog perfused at a constant coronary blood flow. Heart rate was controlled at 150, 190 or 230 beats/minute. 2 Myocardial contractile force and maximal left ventricular d p /d t were not changed by adenosine infusion. 3 The absolute decrease in myocardial O 2 consumption was greater at increasing heart rates whereas the decrease in coronary artery perfusion pressure and peak left ventricular systolic pressure were similar. 4 The results suggest that the reduction in myocardial O 2 consumption produced by adenosine is not related to coronary vasodilatation or to a negative chronotropic or inotropic action, but may be due to a functional shunting of blood flow from high O 2 extracting regions of the myocardium to low O 2 extracting ones and/or to important effects on myocardial substrate utilization.