Hemodynamic effects of PAF-Acether

Abstract

Intravenous PAF-Acether produces extravasation of plasma and systemic hypotension. Blood flow to vital organs, including the kidneys, is markedly reduced as a consequence. This study examines the role of cyclo-oxygenase metabolites and angiotensin II in mediating the hemodynamic effects and the renal consequences of PAF-Acether injection. Indomethacin prevents the reduction of arterial blood pressure during PAF infusion. However, the fall in glomerular filtration and renal plasma flow is not abolished by this treatment: inulin and PAH clearances fall from 42 ± 2 to 30 ± 1ml/min, and from 102 ± 5 to 59 ± 4m1/min, respectively. Similarly, indomethacin does not prevent the fall in urinary sodium excretion. However, when angiotensin II receptors blockade is added to indomethacin, glomerular filtration is not statistically affected during PAF infusion. PAH clearance only decreases from 100 ± 8 to 87 ± 8ml/min. However, the combined administration of indomethacin and saralasin does not prevent the fall in urinary sodium excretion, which decreases from 132 ± 10 to 67 ± 6uEq/min. The results therefore indicate that the vascular effects of PAF-acether are heterogeneous: the peripheral actions require the production of vasodilatory prostaglandins, whereas in the kidney, inhibition of prostaglandins synthesis does not prevent the effect on renal hemodynamics and sodium excretion. It is likely that the vasoconstrictor effect of PAF on renal plasma flow and glomerular filtration results from increased release of angiotensin II, since saralasin prevents those effects. The mechanisms responsible for the dissociation between renal hemodynamics and urinary sodium excretion require further studies.