title: Compression of intramyocardial arterioles during cardiac contraction is attenuated by accompanying venules.
abstract: It was calculated how cardiac contraction influences the luminal cross-sectional area of a maximally dilated coronary arteriole (37-micron inner diameter at a pressure of 35 mmHg) that is accompanied by two equal venules (45-micron inner diameter at a pressure of 17 mmHg), forming a so-called "triad." It was found that, during a contraction with 14% cardiac muscle shortening, arteriolar area is virtually unaffected (increase of 4%) at the expense of a large (55%) decrease in venular area. For comparison, the areas of an unaccompanied arteriole and an unaccompanied venule were calculated to be reduced by 45 and 36%, respectively, demonstrating the "protective effect" on accompanied arterioles in a triad. During contraction, the overall resistance of a system consisting of one arteriole in series with two parallel venules of equal length was calculated to increase about twice as much for nonaccompanied vessels (resistance increases by a factor of 2.8) than for vessels in a triad arrangement (resistance increased by a factor of 1.4). The calculations show that the extravascular (intramyocardial) pressure, which determines vascular area, is not an independent variable as in the intramyocardial pump and waterfall models but depends on the vascular "loading" conditions. Thus the small venular pressure together with the large venular compliance causes the extravascular pressure to remain low during contraction, thereby protecting the stiff arteriole at high pressure. We conclude that the triad arrangement of intramyocardial coronary vessels attenuates the increase in coronary resistance during cardiac contraction and thus has an important functional advantage.
authors.affiliation: Laboratory for Physiology, Vrije Universiteit, Amsterdam, The Netherlands.
authors.forename: M A
authors.initials: MA
authors.lastname: Vis
authors.forename: P
authors.initials: P
authors.lastname: Sipkema
authors.forename: N
authors.initials: N
authors.lastname: Westerhof
mesh_terms: D001160:Arterioles / Q000502:physiology; D003326:Coronary Circulation; D006801:Humans; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D011312:Pressure; D012680:Sensitivity and Specificity; D014655:Vascular Resistance; D014699:Venules / Q000502:physiology