title: Perfusion-induced changes in cardiac O2 consumption and contractility are based on different mechanisms.
abstract: Increased cardiac perfusion results in increased oxygen consumption (VO2) and increased contractility (Gregg phenomenon) in the isolated heart. We investigated whether these two aspects of the Gregg phenomenon are related to coronary flow or arterial pressure. Coronary flow and, thus, arterial pressure were changed in the reference state and during vasoconstriction (3 nM vasopressin) in the Langendorff-perfused rat heart contracting isovolumically (ventricular balloon) at 27 degrees C (n = 5). All hearts showed an increase in developed isovolumic left ventricular pressure (measure of contractility) and in VO2 with increased perfusion. Developed left ventricular pressure depended primarily on arterial pressure, so its relationship with coronary flow was shifted by vasoconstriction. Conversely, VO2 primarily depended on coronary flow, so its relationship with arterial pressure was shifted with vasoconstriction. By use of vasoconstriction (decreased vascular radii), the effects of arterial pressure and wall shear stress (proportional to arterial pressure x radius) should be separable, but the results did not reach significance. Thus contractility is related to arterial pressure or shear stress, whereas VO2 is related to coronary flow. We conclude that the two aspects of the Gregg phenomenon are based on different mechanisms.
authors.affiliation: Laboratory for Physiology, Vrije Universiteit, Amsterdam, The Netherlands. m.dijkman.physiol@med.vu.nl
authors.forename: M A
authors.initials: MA
authors.lastname: Dijkman
authors.forename: J W
authors.initials: JW
authors.lastname: Heslinga
authors.forename: P
authors.initials: P
authors.lastname: Sipkema
authors.forename: N
authors.initials: N
authors.lastname: Westerhof
mesh_terms: D000818:Animals; D001696:Biomechanical Phenomena; D003326:Coronary Circulation; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption; D010477:Perfusion; D011312:Pressure; D051381:Rats; D017208:Rats, Wistar; D014655:Vascular Resistance; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology; D016277:Ventricular Function, Left
chemical_list: D014662:Vasoconstrictor Agents; D014667:Vasopressins