Blood viscosity, hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel

• Published in: Acta anaesthesiologica Scandinavica Vol. 45; no. 3; pp. 371 - 376
• Main Authors: Hilzenrat, N., Arish, A., Yaari, A., Almog, Y., Sikuler, E.
• Format: Journal Article
• Language: English
• Published: Copenhagen Munksgaard International Publishers 01.03.2001; Blackwell
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Biological and medical sciences; Blood Viscosity; Blood Volume; Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis; Controlled bleeding; Haemaccel; Hematocrit; hemodilution; Hemodynamics; Male; Medical sciences; Plasma Substitutes - therapeutic use; Polygeline - therapeutic use; radioactive microspheres; Rats; Rats, Sprague-Dawley; Shock - blood; Shock - physiopathology; Shock - therapy; Splanchnic Circulation; Transfusions. Complications. Transfusion reactions. Cell and gene therapy; vascular hindrance; Vascular Resistance; viscosity; Shock; Viscosity; Intravenous administration; Rat; Rodentia; Splanchnic region; Cardiovascular disease; Hemorrhage; Colloid; Blood; Blood flow; Whole blood; Plasma substitute; Vertebrata; Mammalia; Vascular resistance; Gelatin; Perfusion; Animal; Hemodynamics
• ISSN: 0001-5172; 1399-6576
• DOI: 10.1034/j.1399-6576.2001.045003371.x

Background: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. Methods: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization.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 as 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: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1±9.0 and 3.1±0.5 vs 25.9±6.8 and 2.2±0.9 ml · min−1 · 100 g bw−1, respectively; P<0.05), decreased viscosity (2.8±1.3 vs 3.7±1.3, respectively; P<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.8±1.1 and 40.9±7.6 vs 5.2±1.7 and 61.1±29.5 mmHg · ml−1 · min · 100 g bw, respectively; P<0.05). No significant differences between the groups were observed in vascular hindrance and cardiac output distribution. Conclusion: Volume replacement with Haemaccel, compared to blood, induced increase in systemic and splanchnic blood flows, reflecting mainly changes in viscosity and not in blood vessel geometry. These results suggest no significant difference in overall activation of autoregulation process between volume restitution with blood or Haemaccel.