Maximum myocardial oxygen transport during anemia and polycythemia in dogs.
The purpose of this study was to determine the effect of hematocrit changes on coronary pressure-flow relations during maximum vasodilation to define the relative importance of changes in hemoglobin concentration, blood viscosity, and perfusion pressure in determining maximum myocardial oxygen transport. An anemic group and a polycythemic group of dogs were studied under halothane anesthesia at the hematocrit extremes and after serial exchange transfusions to intermediate hematocrits. Circumflex pressure-flow relations were generated at each hematocrit during maximum pharmacological vasodilation (adenosine 20 micrograms X kg-1 X min-1 or chromonar 8 mg/kg). Maximal coronary vascular conductance (incremental conductance) decreased in an approximately linear fashion with increasing hematocrit. Maximum myocardial oxygen transport showed an "inverted U-shape" relation to hematocrit with the peak occurring at or slightly above normal hematocrit. Hemoglobin concentration, viscosity, and perfusion pressure were all found to be physiologically important determinants of maximal myocardial oxygen transport. Given normal perfusion pressure, arterial oxygen saturation, and myocardial oxygen extraction, we found that maximum myocardial oxygen delivery greatly exceeds the level necessary to supply basal myocardial oxygen needs at all hematocrits studied.
D000241:Adenosine / Q000494:pharmacology; D000740:Anemia / Q000503:physiopathology*; D000818:Animals; D001809:Blood Viscosity; D002866:Chromonar / Q000494:pharmacology; D004285:Dogs; D005260:Female; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D006454:Hemoglobins / Q000378:metabolism; D006706:Homeostasis; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D010477:Perfusion; D011086:Polycythemia / Q000503:physiopathology*; D014664:Vasodilation / Q000187:drug effects
D006454:Hemoglobins; D000241:Adenosine; D002866:Chromonar