Faculty Collaboration Database

Effects of volatile anesthetic agents on in situ vascular smooth muscle transmembrane potential in resistance- and capacitance-regulating blood vessels. Anesthesiology 1998 Apr;88(4):1085-95

Date

05/14/1998

Pubmed ID

9579519

DOI

10.1097/00000542-199804000-00030

Scopus ID

2-s2.0-0031921339 (requires institutional sign-in at Scopus site)   39 Citations

Abstract

INTRODUCTION: This study was designed to compare the inhibitory effect of inhaled volatile anesthetic agents on in situ sympathetic neural versus nonneural regulation of vascular smooth muscle transmembrane potentials as correlates of vascular smooth muscle tone in resistance- and capacitance-regulating blood vessels.

METHODS: Vascular smooth muscle transmembrane potentials were measured in situ with glass microelectrodes in neurally intact, small (200-300 m OD) mesenteric arteries and veins of rats before, during, and after inhaled halothane, isoflurane, or sevoflurane (0.5 or 1.0 minimum alveolar concentration [MAC]). Such transmembrane potentials and their anesthetically induced changes were compared, respectively, with those measured in similar vessel preparations after local sympathetic neural denervation with 6-hydroxydopamine.

RESULTS: In neurally intact vessels, transmembrane potentials (in millivolts, mean +/- SD) before inhalation of the anesthetic agent were -39 +/- 2.8 (artery) and -43 +/- 4.6 (vein). At 1.0 MAC, halothane, isoflurane, and sevoflurane induced respective hyperpolarizations (in millivolts, mean +/- SD) of 9 +/- 3.1, 6 +/- 2.7, and 9 +/- 4.0 in arteries and 6 +/- 4.4, 2.8 +/- 3.0, and 8.7 +/- 5.6 in veins. Sympathetic denervation significantly attenuated these hyperpolarizations (except for venous response to isoflurane). At 0.5 MAC, transmembrane potential responses to all three volatile anesthetic agents were small and not consistently significant in either the intact or denervated vessels.

CONCLUSIONS: In resistance-regulating arteries in situ, inhaled halothane, isoflurane, and sevoflurane (1.0 MAC) attenuate both sympathetic neural and nonneural regulation of vascular smooth muscle transmembrane potentials (and tone). In capacitance-regulating veins in situ, sevoflurane (1.0 MAC) also attenuates both regulatory mechanisms, whereas halothane and isoflurane primarily attenuate nonneural mechanisms. At 0.5 MAC, none of these agents significantly affected either mode of regulation of vascular smooth muscle transmembrane potentials in arteries or veins.

Author List

Yamazaki M, Stekiel TA, Bosnjak ZJ, Kampine JP, Stekiel WJ

Author

Zeljko Bosnjak PhD, MS Emeritus Professor in the Medicine department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Administration, Inhalation
Anesthetics, Inhalation
Animals
Denervation
Halothane
Isoflurane
Male
Membrane Potentials
Mesenteric Arteries
Mesenteric Veins
Methyl Ethers
Muscle, Smooth, Vascular
Rats
Rats, Sprague-Dawley
Vascular Capacitance
Vascular Resistance