Calcium and its role in myocardial cell injury during ischemia and reperfusion

E. Marban; Y. Koretsune; M. Corretti; V. P. Chacko; H. Kusuoka

Calcium and its role in myocardial cell injury during ischemia and reperfusion

E. Marban, Y. Koretsune, M. Corretti, V. P. Chacko, H. Kusuoka

School of Medicine

Research output: Contribution to journal › Article › peer-review

140 Scopus citations

Abstract

Direct measurements of intracellular free Ca²⁺ concentration ([Ca²⁺](i)) were obtained during ischemia and reperfusion in ferret hearts loaded with the Ca²⁺ indicator, the 5,5'-difluoro derivative of 1,2-bis(o-aminophenoxy)ethane-N,N,N',N',-tetraacetic acid. During 15 minutes of ischemia at 37°C, time-averaged [Ca²⁺](i) increased significantly and rapidly during reperfusion. In contrast to metabolic inhibition in isolated muscle or cells, the increase in [Ca²⁺](i) during true ischemia occurs in the absence of a mechanical contracture. After ischemia, contractile function does not recover completely: the hearts are 'stunned'. Our results support the hypothesis that an increase in cellular calcium-loading causes dysfunction in the form of myocardial stunning while leaving unresolved the precise mechanism of the calcium-mediated injury.

Original language	English (US)
Pages (from-to)	IV-17-IV-22
Journal	Circulation
Volume	80
Issue number	6 SUPPL.
State	Published - Dec 1 1989

ASJC Scopus subject areas

Cardiology and Cardiovascular Medicine
Physiology (medical)

Cite this

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title = "Calcium and its role in myocardial cell injury during ischemia and reperfusion",

abstract = "Direct measurements of intracellular free Ca2+ concentration ([Ca2+](i)) were obtained during ischemia and reperfusion in ferret hearts loaded with the Ca2+ indicator, the 5,5'-difluoro derivative of 1,2-bis(o-aminophenoxy)ethane-N,N,N',N',-tetraacetic acid. During 15 minutes of ischemia at 37°C, time-averaged [Ca2+](i) increased significantly and rapidly during reperfusion. In contrast to metabolic inhibition in isolated muscle or cells, the increase in [Ca2+](i) during true ischemia occurs in the absence of a mechanical contracture. After ischemia, contractile function does not recover completely: the hearts are 'stunned'. Our results support the hypothesis that an increase in cellular calcium-loading causes dysfunction in the form of myocardial stunning while leaving unresolved the precise mechanism of the calcium-mediated injury.",

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T1 - Calcium and its role in myocardial cell injury during ischemia and reperfusion

AU - Marban, E.

AU - Koretsune, Y.

AU - Corretti, M.

AU - Chacko, V. P.

AU - Kusuoka, H.

PY - 1989/12/1

Y1 - 1989/12/1

N2 - Direct measurements of intracellular free Ca2+ concentration ([Ca2+](i)) were obtained during ischemia and reperfusion in ferret hearts loaded with the Ca2+ indicator, the 5,5'-difluoro derivative of 1,2-bis(o-aminophenoxy)ethane-N,N,N',N',-tetraacetic acid. During 15 minutes of ischemia at 37°C, time-averaged [Ca2+](i) increased significantly and rapidly during reperfusion. In contrast to metabolic inhibition in isolated muscle or cells, the increase in [Ca2+](i) during true ischemia occurs in the absence of a mechanical contracture. After ischemia, contractile function does not recover completely: the hearts are 'stunned'. Our results support the hypothesis that an increase in cellular calcium-loading causes dysfunction in the form of myocardial stunning while leaving unresolved the precise mechanism of the calcium-mediated injury.

AB - Direct measurements of intracellular free Ca2+ concentration ([Ca2+](i)) were obtained during ischemia and reperfusion in ferret hearts loaded with the Ca2+ indicator, the 5,5'-difluoro derivative of 1,2-bis(o-aminophenoxy)ethane-N,N,N',N',-tetraacetic acid. During 15 minutes of ischemia at 37°C, time-averaged [Ca2+](i) increased significantly and rapidly during reperfusion. In contrast to metabolic inhibition in isolated muscle or cells, the increase in [Ca2+](i) during true ischemia occurs in the absence of a mechanical contracture. After ischemia, contractile function does not recover completely: the hearts are 'stunned'. Our results support the hypothesis that an increase in cellular calcium-loading causes dysfunction in the form of myocardial stunning while leaving unresolved the precise mechanism of the calcium-mediated injury.

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Calcium and its role in myocardial cell injury during ischemia and reperfusion

Abstract

ASJC Scopus subject areas

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