Splanchnic and systemic hemodynamics in portal hypertensive rats during hemorrhage and blood volume restitution.
In portal hypertension the hemodynamic events after episodes of bleeding and blood transfusions may have important pathophysiological and therapeutic implications. The present study was designed to evaluate the effect of hemorrhage and blood restitution on splanchnic and systemic hemodynamics in a rat model of portal hypertension induced by portal vein constriction. In 16 portal hypertensive rats, sequential measurements of arterial and portal pressure were obtained during withdrawal and reinfusion of 15 ml X kg-1 body wt of blood. At the completion of the hemorrhage, a decrease of 16.9% +/- 2.6% in arterial pressure and 27.3% +/- 2.2% in portal pressure was observed. After blood reinfusion, arterial pressure returned to baseline values while portal pressure increased by 20.4% +/- 3.2% (p less than 0.01). This increase in portal pressure was not observed in 5 normal rats that were subjected to the same blood volume changes. Hemodynamic studies using a radioactive microsphere technique revealed that the withdrawal of 15 ml X kg-1 body wt of blood is followed by a decrease in portal venous inflow (6.4 +/- 0.4 vs. 10.4 +/- 0.6 ml X min-1 X 100 g-1 body wt in the control group, p less than 0.01). After blood volume restitution, the portal venous inflow returned to control values while the portal-collateral resistance increased significantly (2.06 +/- 0.13 vs. 1.67 +/- 0.07 mmHg X min X ml-1. 100 g, p less than 0.05). These results indicate that during hypovolemia there is a marked reduction in portal pressure because of a reduction in portal venous inflow. Blood volume restitution returns the portal venous inflow to control values. However, the portal pressure increases beyond control values because of an increase in portal-collateral resistance.
D000818:Animals; D001795:Blood Pressure Determination / Q000379:methods; D001804:Blood Transfusion, Autologous; D001810:Blood Volume; D004195:Disease Models, Animal; D006439:Hemodynamics; D006470:Hemorrhage / Q000503:physiopathology* / Q000628:therapy; D006975:Hypertension, Portal / Q000503:physiopathology* / Q000628:therapy; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013152:Splanchnic Circulation