Portal hypertension and blood viscosity.

Previous studies, exploring the effect of blood viscosity on portal pressure in portal hypertensive humans and animal models, have shown conflicting results. In a series of studies, in portal vein constricted rats, we investigated effects of reduced blood viscosity on the hyperdynamic circulation, portal pressure, and vascular geometry. Blood was withdrawn at a rate of 0.3 mL/min for 15 minutes followed by 15 minutes of stabilization.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 (reflecting vessel geometry) was calculated as resistance/viscosity ratio. In normal and portal hypertensive rats, acute volume replacement with Haemaccel, induced increase in systemic and splanchnic blood flows reflecting mainly changes in viscosity and not in blood vessel geometry. However, 24 hours later, in Haemaccel treated animals, an increased splanchnic arteriolar and porto-collateral vascular hindrance were observed. This indicated vasoconstriction in the porto-collateral vascular bed. The increase in portal venous inflow after acute volume restitution with Haemaccel was prevented by pretreatment with propranolol. Although, caution should be taken in extrapolating these results to humans, we would like to speculate that during a portal hypertensive-related bleeding episode: (1) volume replacement with low viscosity plasma expanders may aggravate the hyperdynamic circulation of portal hypertension. (2) Slow rate volume replacement enables hemodynamic adaptation to occur. (3) Volume replacement maybe more safe in a subject pretreated with propranolol.