Abstract

Right ventricular (RV) failure due to increased RV afterload can be a cause of circulatory compromise. An increase in aortic pressure (Pao) has been reported to improve RV load tolerance. In anesthetized mongrel dogs, we investigated the RV responses to increased afterload, the degree to which RV load tolerance increased with increased Pao, and some of the mechanisms that might be responsible for this. Graded occlusion of the pulmonary artery (PA) was performed to the point of circulatory failure (F). The magnitudo of RV afterload that could be tolerated without F was called the highest load tolerable (HLT). At HLT, PA circumference was reduced by 35.1 ± 3%, and there were increases in RV systolic pressure (from 27.5 ± 0.2 to 63.2 ± 3.4 torr, P < .005), RV diastolic pressure (from 4.2 ± 0.5 to 6.1 ± 0.8 torr, P < .05), systolic and diastolic myocardial segment length in both inflow and outflow tracts (by approximately 10%, P < .05), and right coronary arterial blood flow (Q̇ca, by approximately 60%, P < .01). Regional contractility as measured by percent chord shortening, maximum velocity of chord shortening, and time to maximum velocity of chord shortening was unchanged at HLT. With occlusion of the descending aorta (AO), Pao increased from 82.7 ± 3.7 to 143.3 ± 9.3 torr ( P < .01), and there were no changes in baseline RV pressures, chord lengths, contractility, or Q̇ca. Following AO, RV load tolerance increased in that at HLT, PA circumference could be reduced more (by 42.0 ± 3.5%, P < .05). RV systolic pressure (73.9 ± 4.2 torr, P < .01) and diastolic pressure (7.7 ± 0.7 torr, P < .01) pressures were even greater at HLT. However, this was not associated with increased Q̇ca, contractility, nor with significant changes in diastolic or systolic myocardial segment lengths compared to control at HLT. Measurements of intramyocardial pH failed to reveal any evidence of myocardial ischemia at HLT or F. We have confirmed that increased aortic prossure leads to greater RV load tolerance, and conclude that this need not be associated with an increase in contractility, right coronary arterial inflow, or to decreased myocardial ischemia.

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