Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Evidence for subendocardial ischemia despite residual vasodilator reserve.

Abstract

SUMMARY. Right ventricular failure during acute pressure overload has been attributed to ischemia which occurs when maximal coronary vasodilation is achieved so that further increases in myocardial blood flow cannot occur. To test the hypothesis that coronary vasodilator reserve is exhausted during acute right ventricular pressure overload, right and left ventricular myocardial blood flow was measured in 14 awake dogs during progressive pulmonary artery occlusion; coronary vasodilator reserve was tested by infusion of adenosine (4 [iM/kg per min) before and during pulmonary artery occlusion. Right ventricular myocardial blood flow rose from 0.77 ± 0.09 ml/min per g (mean ± SEM) during control conditions to 1.69 ± 0.26 ml/min per g during moderate pulmonary artery occlusion (P < 0.01). With further pulmonary artery occlusion to cause increased right ventricular end-diastolic pressure and decreased aortic pressure, a selective decrease in myocardial blood flow to the right ventricular subendocardium was observed, and the right ventricular subendocardial-tosubepicardial blood flow ratio fell from 1.36 ± 0.14 to 0.77 ± 0.06 (P < 0.05). With restoration of mean aortic pressure to control levels, right ventricular systolic pressure increased, right ventricular end-diastolic pressure decreased, and the right ventricular subendocardial-to-subepicardial ratio increased to 1.36 ± 0.18 (P < 0.01). Adenosine infusion during pulmonary artery occlusion in five dogs caused an increase in mean right ventricular blood flow (1.11 ± 0.10 to 2.25 ± 0.30; P < 0.05). This increase was most marked in the outer layers but, nevertheless, was also significant in the subendocardium. These data indicate that acute severe right ventricular pressure overload may be associated with right ventricular subendocardial hypoperfusion, even when coronary vasodilator reserve is not exhausted. (Circ Res 51: 196-204, 1982 ) DURING increased right ventricular systolic pressure, the determinants of right ventricular oxygen requirements increase (Love et al., 1963;Aukland et al., 1967;Brooks et al., 1971). Since increased systolic compression of the intramural coronary vessels during right ventricular systolic hypertension effectively decreases the perfusion pressure gradient between the aorta and right ventricle, an increase in right ventricular myocardial blood flow can only occur by coronary vasodilation and a decrease in coronary vascular resistance (Cross, 1962;Fixler et al., 1973). Brooks et al., (1971) have proposed that right ventricular myocardial ischemia may occur when maximal coronary vasodilation has been achieved so that further increases in right ventricular myocardial oxygen demands cannot be satisfied by further increases in myocardial blood flow. These investigators demonstrated in open-chest, anesthetized dogs that by mechanically increasing perfusion in the right coronary artery, right ventricular failure due to acute pulmonary artery constriction could be reversed without altering the degree of pulmonary artery constriction. Fixler...

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