Acute hemodynamic changes following hemorrhage and volume restitution, using a low viscosity plasma expander, in anesthetized portal hypertensive rats

Background/Aim: The aim of this study was to examine, in a portal hypertens ive rat model, the hemodynamic changes following hemorrhage and volume rest itution 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 Under ketamine anesthesia, blood was withdrawn at a constant rate of 0.3 ml/min, for 15 min followed by 15 min of stabilization.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 Haemacce l 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, s ignificant reductions in arterial pressure and portal pressure were observe d. Volume replacement with blood was accompanied by increased mean arterial pressure and portal pressure to baseline. Arterial pressure following volu me 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, respect ively; p<0.05). Volume replacement with Haemaccel, compared to blood, was f ollowed by increased cardiac output and portal venous inflow (39.3+/-11.6 a nd 4.4+/-1.5 vs 28.9+/-3 and 2.9+/-0.8 ml.min(-1) 100 g bw(-1), respectivel y; p<0.05), decreased hematocrit and viscosity (29.3+/-3.8% and 2.8+/-1.3 v s 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.ml(-1).min 100 g b vv, respectively; p<0.05). There were no significant changes in vascular hindrance in any vascular beds bet ween the two groups. Conclusion: In this model, volume replacement with Haemaccel induced an inc rease in cardiac output and portal venous inflow thus preventing the reduct ion in portal pressure which might be expected when viscosity is reduced.