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The Mechanisms of Impaired Tolerance to Ischemia in Hypertrophied Heart

Research Project

Project/Area Number 05671117
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Thoracic surgery
Research InstitutionOsaka University

Principal Investigator

SHIMAZAKI Yasuhisa (1994)  Osaka University Medical Assistant Professor, 医学部, 助教授 (60116043)

川田 博昭 (1993)  大阪大学, 医学部, 助手 (40234075)

Co-Investigator(Kenkyū-buntansha) FUKUSHIMA Norihide  Osaka University Medical Assistant, 医学部, 助手 (30263247)
新谷 英夫  大阪大学, 医学部, 助手 (10243221)
島崎 靖久  大阪大学, 医学部, 講師 (60116043)
Project Period (FY) 1993 – 1994
Project Status Completed (Fiscal Year 1994)
Budget Amount *help
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥1,300,000 (Direct Cost: ¥1,300,000)
Keywordscardiac hypertrophy / intracellular calcium / intracellular sodium / intracellular pH / cardiac ischemia / myocardial protection / c-myc / 心筋保進
Research Abstract

The aim of this study was to investigate the mechanism of the impaired tolerance to ischemia in hypertrophied heart and to find out how to protect hypertrophied hearts against ischemia reperfusion injury.
1)The method for the measurement of intracellular Ca, Na and pH was established in isolated rat whole heart.
2)Hypertrophied rat heart model was established by the shunting between abdominal aorta and inferior vena cave in adult male S-D rats. the weight of the hearts became two times as much as the normal hearts after 4 weeks of the shunting operation.
3)In hypertrophied rat hearts, intracellular calcium activity measured by fura-2 fluorescence was significantly increased than in normal heart after 20 minutes of normothermic ischemia.
4)Terminal cardioplegia attenuated the increased Ca fluorescence in hypertrophied hearts during reperfusion. Myocardial ATP content and the total amout of adenine nucleotide were maintained by using terminal cardioplegia both in normal and hypertrophied hearts.
5)Intracellular sodium increased after 20 minutes of ischemia and mormalized after 10 minutes of reperfusion.
6)In hypertrophied hearts, immunohistochemical examination revealed that c-myc (one of the oncogenes which regulates the hypertrophy of the myocytes) appeared 2 hours after shunting operation and showed significant hypertrophy 2 weeks after shunting operation, suggesting that the gene expression of hypertrophy occurrs just after the initiation of volume overload.

Report

(3 results)
  • 1994 Annual Research Report   Final Research Report Summary
  • 1993 Annual Research Report

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Published: 1993-04-01   Modified: 2016-04-21  

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