title: Venous waterfalls in coronary circulation.
abstract: Several studies of flow through collapsible tubing deformed by external pressures have led to a concept known as the "vascular waterfall". One hallmark of this state is a positive zero-flow pressure intercept (Pe) in flow-pressure curves. This intercept is commonly observed in the coronary circulation, but in blood-perfused beating hearts a vascular waterfall is not the only putative cause. To restrict the possibilities, we have measured flow-pressure curves in excised non-beating rabbit hearts in which the coronary arteries were perfused in a non-pulsatile way with a newtonian fluid (Ringers solution) containing potent vasodilator drugs. Under these circumstances, vascular waterfalls are believed to be the only tenable explanation for Pe. In physical terms the waterfall is a region where the vessel is in a state of partial collapse with a stabilized intraluminal fluid pressure (Pw). It is argued that the most probable site of this collapse was the intramural veins just before they reached the epicardial surface. In accord with the waterfall hypothesis, Pe increased as the heart became more edematous, but flow-pressure curves also became flatter, implying multiple waterfalls with differing Pws, leading to complete collapse of some of the venous channels. The principal compressive force is believed to have been the interstitial fluid pressure as registered through a needle (Pn) implanted in the left ventricular wall, but a small additional force (Ps) was probably due to swelling of interstitial gels. A method is presented for estimating Ps and Pw. Unlike rubber tubing, blood vessels are both collapsible and porous. Apparently because of increased capillary filtration, Pn was found to increase linearly with the perfusion pressure. Thus, Pw was not the same at all points on the flow-pressure curve. This finding has interesting implications with respect to the concept of coronary resistance.
authors.affiliation: Department of Pharmacology and Toxicology, Dartmouth Medical School, Hanover, New Hampshire 03756.
authors.forename: R E
authors.initials: RE
authors.lastname: Gosselin
authors.forename: S M
authors.initials: SM
authors.lastname: Kaplow
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D001808:Blood Vessels / Q000502:physiology; D003326:Coronary Circulation / Q000502:physiology*; D006321:Heart / Q000502:physiology; D008955:Models, Cardiovascular; D011817:Rabbits; D012039:Regional Blood Flow / Q000502:physiology*