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.

Dependence of Intramyocardial Pressure and Coronary Flow on Ventricular Loading and Contractility: A Model Study

“…Main limitation of our model with respect to the model presented by Vis et al .,26,27 lies in neglecting the direct contribution of tissue stress to the extravascular pressure and effective compliance of the coronary vessel. The approach of Vis et al .…”

“…Vis et al 26,27. extended the model for interaction between the vessel and the cardiac wall, by assuming that the coronary vessel is subject to an extravascular pressure that depends both on intramyocardial pressure and local tissue stress.…”

Wall thickness of coronary vessels varies transmurally in the LV but not the RV: implications for local stress distribution

“…Hence, their diameter is a function of transmural pressure, which is the difference between coronary blood pressure and IMP. The latter increases in systole, which causes an increase in coronary blood pressure, which in turn decreases the pressure gradient on the arterial side of the coronary network and increases the pressure gradient on the venous side (2,10,21,30,34,41). There is a substantial difference in the effect of cardiac contraction on intramyocardial vessels between the subepicardial and subendocardial layers.…”

Systolic coronary flow impediment in the dog: role of ventricular pressure and contractility

“…We therefore performed a new study to investigate the effects of LVP and contractility on coronary arterial inflow in the in situ dog heart, and examined the effect of low and high LVP over a wide range of ventricular volumes for two different inotropic states obtained without pharmacological interventions and after suppression of autoregulation obtained with maximal vasodilatation. Since the distal microvessels play a key role in the coronary flow impediment in systole, collapsing under the effect of the increased myocardial tension (Downey & Kirk, 1975;Vis et al 1997a;Vis, Sipkema & Westerhof, 1997b;Bruinsma et al 1988), and since, in the presence of a normal perfusion pressure, vasodilatation can cause an increase in pressure in the distal microvessels (Chilian, Layne, Klausner, Eastham, Marcus, 1989;Fujii, Nuno, Lamping, Dellsperger, Eastham, Harrison, 1992;Vis et al 1997a), thereby preventing or limiting the reduction of vascular lumen in systole (Vis et al 1997b), care was taken to keep perfusion pressure low enough to prevent such an increase.…”