VASOCONSTRICTION DURING ACUTE HYPERVOLEMIC HEMODILUTION IN HYPERTENSIVE PATIENTS IS NOT PREVENTED BY CALCIUM BLOCKADE

The reduction of blood viscosity by moderate acute hypervolemic hemodi lution in untreated hypertensives can be associated with a secondary v asoconstriction. The aim of this study was to examine whether a vasodi lating therapy prevents this hemodynamic reaction. Twelve hypertensive patients (WHO stage II) were treated with the vasoselective calcium c hannel blocker isradipine in a placebo-controlled, double-blind, cross over study. Acute hypervolemic hemodilution was performed twice: at th e end of the placebo period and after two months of treatment. Hemodil ution was achieved by the intravenous infusion of 1000 mL saline over a 10- to 15-minute period. Arterial blood pressure, heart rate, cardia c output (dye dilution), renal blood flow, glomerular filtration, natr iuresis, hematocrit, whole blood, and plasma viscosity were assessed b efore and after infusion. Flow resistance and vascular hindrance in th e central and renal circulation were calculated. Acute hemodilution as sociated with a significant reduction of blood (P<0.01) and plasma (P< 0.01) viscosity did not influence the mean arterial pressure and cardi ac output. Consequently, the total flow resistance remained unchanged. However, as a result of hemodilution, the calculated vascular hindran ce index in the systemic circulation increased, indicating a vasoconst rictive reaction, both with placebo (from 5.22 to 6.07 U x mPa(-1) x s (-1), P<0.05) and during chronic treatment with calcium blockade (from 3.75 to 4.22 U x mPa(-1) x s(-1), P<0.02). Vasoconstriction was not o bserved in the renal circulation, either during the placebo or active treatments. The results of this study indicate that the systemic vasoc onstriction evoked by the acute moderate hypervolemic hemodilution in hypertensive patients was not prevented by a calcium channel blockade.