Nir Hilzenrat1, Arieh Yaari, Emanuel Sikuler. 1. Liver Research Laboratory, The Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Abstract
BACKGROUND AND AIM: In portal hypertensive rats, hemorrhage and acute volume restitution with Haemaccel induced increased cardiac output and portal venous inflow. In the present study, the late hemodynamic effects of this procedure were explored. METHODS: Portal hypertension was induced by portal vein constriction. Blood was withdrawn 11.2 +/- 3.2 days later, at a rate of 0.3 mL/min, for 15 min, followed by 15 min of stabilization. Haemaccel or blood were infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after 24 h, using radioactive microspheres. Viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as resistance/viscosity ratio. RESULTS: Blood viscosity of the Haemaccel group (n = 11), was lower than in the blood group (n = 11): 2.7 +/- 0.2 versus 4.0 +/- 0.4 (P < 0.01). Arterial pressure, cardiac output, peripheral resistance, portal pressure, portal venous inflow and splanchnic arteriolar resistance were not significantly different. Splanchnic arteriolar and portocollateral hindrance were higher in the Haemaccel group (11.7 +/- 5.3 and 1.5 +/- 0.6 vs 7.7 +/- 3.0 and 0.9 +/- 0.4 mmHg x min x 100 gram body weight/mL, respectively, P < 0.05). CONCLUSION: In portal hypertensive rats, vital organs perfusion, 24 h after hemorrhage and isovolemic volume restitution with Haemaccel and blood, was similar. However, in Haemaccel-transfused animals, a reduction in vascular hindrance, indicating vasoconstriction, was observed in the splanchnic organs, which drain into the portal circulation. Vasoconstriction of the portocollateral vascular bed was observed as well. We suggest that slow-rate volume replacement during a portal-hypertensive-related bleeding episode enables hemodynamic adaptation to occur. Thus, undesirable hyperdynamic changes, which may aggravate secondary bleeding, are attenuated. Copyright 2002 Blackwell Publishing Asia Pty Ltd
BACKGROUND AND AIM: In portal hypertensiverats, hemorrhage and acute volume restitution with Haemaccel induced increased cardiac output and portal venous inflow. In the present study, the late hemodynamic effects of this procedure were explored. METHODS: Portal hypertension was induced by portal vein constriction. Blood was withdrawn 11.2 +/- 3.2 days later, at a rate of 0.3 mL/min, for 15 min, followed by 15 min of stabilization. Haemaccel or blood were infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed after 24 h, using radioactive microspheres. Viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as resistance/viscosity ratio. RESULTS: Blood viscosity of the Haemaccel group (n = 11), was lower than in the blood group (n = 11): 2.7 +/- 0.2 versus 4.0 +/- 0.4 (P < 0.01). Arterial pressure, cardiac output, peripheral resistance, portal pressure, portal venous inflow and splanchnic arteriolar resistance were not significantly different. Splanchnic arteriolar and portocollateral hindrance were higher in the Haemaccel group (11.7 +/- 5.3 and 1.5 +/- 0.6 vs 7.7 +/- 3.0 and 0.9 +/- 0.4 mmHg x min x 100 gram body weight/mL, respectively, P < 0.05). CONCLUSION: In portal hypertensiverats, vital organs perfusion, 24 h after hemorrhage and isovolemic volume restitution with Haemaccel and blood, was similar. However, in Haemaccel-transfused animals, a reduction in vascular hindrance, indicating vasoconstriction, was observed in the splanchnic organs, which drain into the portal circulation. Vasoconstriction of the portocollateral vascular bed was observed as well. We suggest that slow-rate volume replacement during a portal-hypertensive-related bleeding episode enables hemodynamic adaptation to occur. Thus, undesirable hyperdynamic changes, which may aggravate secondary bleeding, are attenuated. Copyright 2002 Blackwell Publishing Asia Pty Ltd