Changes in regional vascular capacitance during prostacyclin-induced cardiac vagal reflex in pigs

The purpose of this study was to determine the effects of the prostaglandin I2 (prostacyclin; PGI2)-induced cardiac vagal reflex on intestinal and liver blood volumes and the intestinal vascular pressure-volume (P-V) relationship. In anesthetized pigs, blood volumes were measured by blood-pool scintigraphy. Portal venous pressure was varied by graded inflation of a portal vein constrictor to determine the intestinal vascular P-V relationship. Proximal right coronary infusion of PGI2 at a rate of 0.15 micrograms.kg-1.min-1 for 6 min increased intestinal blood volume by 7.0 +/- 1.2% (P < 0.01, means +/- SE) and shifted the intestinal vascular P-V relationship away from the pressure axis (i.e., a volume increase at a given venous pressure). This change was associated with decreases in liver blood volume and left ventricular end-diastolic pressure by 4.5 +/- 1.2 (P < 0.01) and 17 +/- 2% (P < 0.05), respectively. PGI2 also reduced central venous pressure by 16 +/- 2% from 3.2 +/- 0.5 mmHg (P < 0.05) and portal venous pressure by 7.0 +/- 0.6% from 7.6 +/- 0.6 mmHg (P < 0.05). These responses were abolished by bilateral vagotomy. The results demonstrate that intracoronary PGI2 infusion increases intestinal blood volume. This increase is mediated by a cardiac vagal reflex. The PGI2-induced shift in the intestinal vascular P-V relationship suggests that intestinal blood volume increases by an active change in vascular capacitance, whereas reductions in liver blood volume and left ventricular end-diastolic pressure appear to be due to passive mechanisms related to the shift of blood volume to the intestinal circulation.