Acute hemodynamic changes following hemorrhage and volume restitution, using a low viscosity plasma expander, in anesthetized portal hypertensive rats.
OBJECTIVE
The aim of this study was to examine, in a portal hypertensive rat model, the hemodynamic changes following hemorrhage and volume restitution with blood and Haemaccel (a low viscosity, volume expander).


METHODS
Portal hypertension was induced by portal vein constriction. Under ketamine anesthesia, blood was withdrawn at a constant rate of 0.3 ml/min, for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio.


RESULTS
Twelve rats were studied in each group. During blood withdrawal, significant reductions in arterial pressure and portal pressure were observed. Volume replacement with blood was accompanied by increased mean arterial pressure and portal pressure to baseline. Arterial pressure following volume replacement with Haemaccel was lower and portal pressure was higher than baseline (128+/-16 and 17.1+/-3.9 vs 146+/-13 and 15.9+/-3.0 mmHg, respectively; p<0.05). Volume replacement with Haemaccel, compared to blood, was followed by increased cardiac output and portal venous inflow (39.3+/-11.6 and 4.4+/-1.5 vs 28.9+/-3 and 2.9+/-0.8 ml x min(-1) x 100 g bw(-1), respectively; p<0.05), decreased hematocrit and viscosity (29.3+/-3.8% and 2.8+/-1.3 vs 35.7+/-3.4% and 4.0+/-1.3, respectively; p<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.6+/-1.4 and 29.2+/-14.0 vs 5.0+/-1.4 and 43.9+/-12.7 mmHg x ml(-1) x min x 100 g bw, respectively; p<0.05). There were no significant changes in vascular hindrance in any vascular beds between the two groups.


CONCLUSIONS
In this model, volume replacement with Haemaccel induced an increase in cardiac output and portal venous inflow, thus preventing the reduction in portal pressure which might be expected when viscosity is reduced.
Hilzenrat
N
N
Department of Medicine B, The Soroka Medical Center, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva, Israel.
Arish
A
A
Yaari
A
A
Sikuler
E
E
D000818:Animals; D001794:Blood Pressure; D001803:Blood Transfusion; D001809:Blood Viscosity; D002302:Cardiac Output; D006439:Hemodynamics; D006975:Hypertension, Portal / Q000150:complications* / Q000503:physiopathology*; D008297:Male; D010952:Plasma Substitutes / Q000627:therapeutic use*; D011097:Polygeline / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D014655:Vascular Resistance
D010952:Plasma Substitutes; D011097:Polygeline