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2017 Fiscal Year Final Research Report

Effects of Anesthetics on TRPC channel mediated myocardial protection

Research Project

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Project/Area Number 15K10534
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Anesthesiology
Research InstitutionShiga University of Medical Science

Principal Investigator

Hirotoshi KITAGAWA  滋賀医科大学, 医学部, 教授 (50252391)

Co-Investigator(Renkei-kenkyūsha) YAMAZAKI TOJI  滋賀医科大学, 医学部, 非常勤講師 (20116122)
KOJIMA AKIKO  滋賀医科大学, 医学部, 助教 (50447877)
MATSUURA HIROSHI  滋賀医科大学, 医学部, 教授 (60238962)
TAKAHASHI KAN  滋賀医科大学, 医学部, 准教授 (80346014)
Project Period (FY) 2015-04-01 – 2018-03-31
Keywords吸入麻酔薬 / TRPCチャネル / 心筋保護 / 虚血再灌流傷害 / マイクロダイアリシス
Outline of Final Research Achievements

Using microdialysis technique, we monitored myocardial interstitial myoglobin in the ischemic region of anesthetized rat during ischemia and after reperfusion. In the vehicle, myoglobin levels increased during ischemia and after reperfusion. 2-APB, SKF96365, a TRPC channel blocker, suppressed the increase in dialysate myoglobin levels during ischemia and reperfusion. Sevoflurane also reduced dialysate myoglobin levels during ischemia and reperfusion. In transverse aortic constriction (TAC) model rats with TRPC channel activation, myoglobin levels also increased during ischemia and after reperfusion. These were further suppressed than those in wild type rats with pretreatment of 2-APB, SKF96365 and sevoflurane. These results suggested that TRPC channels plays a significant role in cardiomyocyte injury during ischemia and after reperfusion. Furthermore, sevoflurane might exert an in vivo myocardial protective effect during ischemia and after reperfusion via TRPC channels.

Free Research Field

周術期管理学

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Published: 2019-03-29  

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