Toshihiro Yorozuya⁽¹⁾, Naoto Adachi⁽²⁾, Masao Soutani⁽³⁾, Kazuo Nakanishi⁽⁴⁾, Kentaro Dote⁽⁵⁾, Shigeo Kimura⁽⁶⁾, Takumi Nagaro⁽⁷⁾, Tatsuru Arai^{(8)
(1)(2)(3)(7)(8)}Ehime-university School of Medicine - Japan
^(4)(5)(6)Ehime university School of Medicine - Japan

	[Pharmacology]	[Cardiolovascular Diseases]

INTRODUCTION

There are many studies both morphological and functional, that glucocorticoids improve ischemia-induced myocardial injury ^(1-4). This action is speculated to be caused by the preservation of cellular functions in ischemia, which results in prolongation of the period of myocardial viability. Although glucocorticoids have been demonstrated to improve lactate imbalance and prevent leakage of intracellular enzymes caused by ischemia ^(3,4), the mechanism underlying this protection has not been clarified. Considering the improvement of lactate balance during continuing coronary occlusion, it is likely that glucocorticoids change metabolism in the anaerobic state. Since adenosine 5´-triphosphate (ATP) provides energy for contraction and maintains membrane functional integrity, we investigated the effect of dexamethasone, a pure glucocorticoid, on the hypoxic reduction of ATP in the mouse heart.

Discussion Board

Any Comment to this presentation?

[ABSTRACT] [INTRODUCTION] [MATERIAL & METHODS] [RESULTS] [FIGURES] [DISCUSSION] [CONCLUSIONS] [BIBLIOGRAPHY] [Discussion Board]

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	[Pharmacology]	[Cardiolovascular Diseases]

Toshihiro Yorozuya, Naoto Adachi, Masao Soutani, Kazuo Nakanishi, Kentaro Dote, Shigeo Kimura, Takumi Nagaro, Tatsuru Arai
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Last update: 14/01/00