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Am J Physiol Heart Circ Physiol 273: H618-H627, 1997;
0363-6135/97 $5.00
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AJP - Heart and Circulatory Physiology, Vol 273, Issue 2 618-H627, Copyright © 1997 by American Physiological Society

ARTICLES

Anesthetics alter relative contributions of NO and EDHF in rat cremaster muscle microcirculation

A. L. Loeb, I. Godeny and D. E. Longnecker
Department of Anesthesia, University of Pennsylvania, Philadelphia 19104-4283, USA.

The contributions of the vasodilators nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) were investigated in the rat cremaster muscle microcirculation during halothane, isoflurane, or ketamine anesthesia. After inhibition of prostaglandin synthesis with indomethacin, changes in diameter of fourth-order arterioles to acetylcholine (ACh) or bradykinin (BK) were studied in the presence or absence of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, and/or 20 mM K+, an inhibitor of EDHF action. L-NMMA inhibited ACh- and BK-induced vasodilation during isoflurane but not halothane or ketamine anesthesia. Superfusion of the muscle with buffer containing 20 mM K+ dilated arterioles. EDHF was responsible for most of the NO-independent response to ACh, because 20 mM K+ unmasked ACh-stimulated, NO-dependent relaxation during halothane or ketamine anesthesia. However, 20 mM K+ did not inhibit BK-induced vasodilation during halothane or ketamine anesthesia. Our data suggest that anesthetics can alter the balance between NO and EDHF vasodilation in the microcirculation and that NO-dependent mechanisms are enhanced and EDHF action inhibited during isoflurane anesthesia.


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