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From the Departments of *Anesthesiology and Pain Medicine, and
Cardiology, Gifu University Graduate School of Medicine, Gifu City, Gifu;
Department of Anesthesia, Chubu Rosai Hospital, Nagoya; and
Department of Nutrition and Food Science, Faculty of Home Economics, Gifu Women's University, Gifu, Japan.
Address correspondence and reprint requests to Hiroki Iida, MD, Department of Anesthesiology and Pain Medicine, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu City, Gifu 501-1194, Japan. Address e-mail to iida{at}gifu-u.ac.jp.
BACKGROUND: The potent vasodilators nicardipine and prostaglandin E1 (PGE1) are useful for the treatment of systemic hypertension or pulmonary hypertension during aortic surgery.
METHODS: 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·kg1·min1], or PGE1 [at 0.1 or 1.0 µg·kg1·min1]), just after aortic clamping, 20 min after clamping, and at 060 min after unclamping.
RESULTS: 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.
CONCLUSIONS: The larger doses of nicardipine, but neither dose of PGE1, attenuated aortic unclamping-induced sustained cerebral pial arteriolar constriction.
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