The Comparative Effects of Intravenous Nicardipine and Prostaglandin E1 on the Cerebral Pial Arteriolar Constriction Seen After Unclamping of an Aortic Cross-Clamp in Rabbits

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The potent vasodilators nicardipine and prostaglandin E1 (PGE1) are useful for the treatment of systemic hypertension or pulmonary hypertension during aortic surgery.


We measured cerebral pial arteriolar diameters, using a rabbit closed cranial window preparation: before (baseline) and 15 min after the start of an IV infusion (preclamp) (0.9% saline [control group], nicardipine [at 0.1, 1.0, or 10 μg·kg−1·min−1], or PGE1 [at 0.1 or 1.0 μg·kg−1·min−1]), just after aortic clamping, 20 min after clamping, and at 0–60 min after unclamping.


In the control group, a significant decrease in diameter persisted for at least 60 min after unclamping (maximum [at 60 min], −16% for large [≥75 μm], and −27% for small [<75 μm] arterioles versus baseline). Although the aortic unclamping-induced vasoconstriction was unaffected under the smallest dose of nicardipine, it was significantly attenuated under larger doses in both large and small arterioles (residual vasoconstriction, −10% and −6% for large and −18% and −10% for small arterioles; at 60 min). The pial arteriolar constriction observed at 5 min or more after unclamping in the control group was not altered by PGE1 in either large or small arterioles.


The larger doses of nicardipine, but neither dose of PGE1, attenuated aortic unclamping-induced sustained cerebral pial arteriolar constriction.

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