1998 Fiscal Year Final Research Report Summary
Mechanisms of anesthetics on in situ normotensive vs hypertensive rat mesenteric vascular smooth muscle transmembrane potentials
Project/Area Number |
09671549
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
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Research Institution | Toyama Medical and Pharmaceutical University |
Principal Investigator |
YAMAZAKI Mitsuaki Toyama Medical and Pharmaceutical University, University Hospital, Intensive Care Unit, Associate Professor, 附属病院, 講師 (70158145)
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Co-Investigator(Kenkyū-buntansha) |
SHIBUYA Nobuko Toyama Medical and Pharmaceutical University, University Hospital, Anesthesiolog, 附属病院, 講師 (40178926)
HATAKEYAMA Noboru Toyama Medical and Pharmaceutical University, University Hospital, Operating The, 附属病院, 助手 (70251907)
ITO Yusuke Toyama Medical and Pharmaceutical University, Faculty of Medicine, Anesthesiolog, 医学部, 教授 (70018307)
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Project Period (FY) |
1997 – 1998
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Keywords | vascular smooth muscle / transmembrane potential / isoflurane / sevoflurane / propofol / WKY rat / SHR rat / potassium channel |
Research Abstract |
Since tight linear coupling exists between vascular smooth muscle (VSM) transmembrane potential (Em) and active VSM tone, such hyperpolarization reflects a vasorelaxation. In normotensive and hypertensive rats under basal anesthesia, we externalized a loop of jejunum containing mesenteric arteries and veins through a midline laparotomy and superfused them with physiological salt solution. Ems were recorded from in situ mesenteric resistance (arteries) and capacitance (veins) vessels with or without denervation (by 6- hydroxydopamine) using glass microelectrode. In normotensive rats, inhaled anesthetics (isoflurane, sevoflurane) and ketamine hyperpolarized in both mesenteric arteries and veins. Inhaled anesthetics attenuated both sympathetic neural and nonneural regulation of VSM transmembrane potentials ( and tone). Inhaled anesthetics hyperpolarized in hypertensive rats more negative than in normotensive rats. Selective inhibitors of each of four types of potassium channels known to exist in VSM were administered in superfusate of the vessel preparations (in normotensive rats) to assess their effects on isoflurane-mediated hyperpolarization. Isoflurane-mediated hyperpolarization of VSM can be attributed in part to an enhanced (or maintained) opening of calcium-activated and adenosine triphosphate sensitive potassium channels but not voltage-dependent or inward rectifier potassium channels.
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