Modulation of vascular capacitance by angiotensin and nitroprusside: a mechanism of changes in pericardial pressure.

Abstract

The aim ofthe present study was to test the hypothesis that vasoactive drugs may modify left ventricular diastolic function by shifting blood between the systemic vascular bed and the heart, thereby changing pericardial and left ventricular pressure. The experiments were done in 10 open-chest, anesthetized, previously splenectomized dogs in which changes in pericardial surface pressure in response to intravenous sodium nitroprusside and angiotensin were related to changes in blood volume in the abdominal region. Blood volume was determined by blood pool scintigraphy (99mTc) and regions of interest were drawn in the liver and in the mesenteric area. Angiotensin was infused at rates that were adjusted to increase mean aortic pressure by 20 and 30 mm Hg, and nitroprusside was infused at rates to decrease mean aortic pressure by 30 and 50 mm Hg. Angiotensin increased pericardial pressure by 3 and 5 mm Hg at the respective doses and there were increments in left ventricular end-diastolic pressure (LVEDP) and left ventricular diameter (sonomicrometry). Angiotensin decreased blood volume in the mesenteric region by 14% and 17%, but did not significantly change blood volume in the liver region. Angiotensin increased portal venous pressure and decreased mesenteric blood volume, suggesting decreased mesenteric venous compliance. Nitroprusside had opposite effects: pericardial pressure was decreased by 5.5 and 6.5 mm Hg by the respective doses. The doses of nitroprusside increased blood volume in the mesenteric region by 14% and 20%, but did not significantly change blood volume in the liver region. Nitroprusside decreased portal pressure and increased mesenteric blood volume, suggesting increased mesenteric venous compliance. Changes in pericardial pressure with the two drugs varied inversely with changes in blood volume in the mesenteric region. In conclusion, angiotensin and nitroprusside change LVEDP by changing pericardial pressure. The two drugs had opposite effects on venous capacitance in the abdominal region. Changes in pericardial pressure varied inversely with changes in mesenteric blood volume. Thus, we propose that the mechanism whereby vasoactive drugs alter pericardial pressure is by shifting blood between the systemic venous bed and the heart, thereby changing heart size and necessarily pericardial pressure. Circulation 76, No. 4, 875-883, 1987

Deterioration of Left Ventricular Chamber Performance After Bed Rest

“…A similar leftward displacement of the diastolic P/V curve has been observed after vasodilator 25,26 administration, suggesting that peripheral pooling itself might modify LV diastolic function. Such drugs alter pericardial pressure by shifting blood between the heart and the systemic venous capacitance, thereby changing heart size and, necessarily, pericardial pressure.…”

Effects of Vasodilation in Heart Failure With Preserved or Reduced Ejection Fraction

“…Reduction in LV filling pressure with nitrates are complex and may be due to improvement in afterloaddependent relaxation delay, decrease in chamber volume from venodilation, acute improvement in diastolic compliance, or relief of pericardial constraint (6,7,(23)(24)(25). Absent volume data obtained at the time of catheterization, we cannot determine the relative roles these mechanisms played in the current study.…”

Systemic vascular effects of acute electrical baroreflex stimulation

“…The effects of BAT were also assessed in the presence of SNP to determine if the effects would be additive. Infusion of the arterial and venous (32) vasoconstrictor, angiotensin II (ANG II), allowed BAT to be tested in the presence of substantial vasoconstriction. We hypothesized that the application of BAT would increase abdominal blood volume (as assessed by the Brooksby-Donald technique), that the magnitude of this change might be smaller during the infusion of SNP, and that the effect of BAT might be greater when blood had been mobilized from the splanchnic to the central circulation during the ANG II infusion (34).…”