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Research Article Free access | 10.1172/JCI117216

Alpha 1-adrenoceptor activation mediates the infarct size-limiting effect of ischemic preconditioning through augmentation of 5'-nucleotidase activity.

M Kitakaze, M Hori, T Morioka, T Minamino, S Takashima, H Sato, Y Shinozaki, M Chujo, H Mori, and M Inoue

First Department of Medicine, Osaka University School of Medicine, Japan.

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First Department of Medicine, Osaka University School of Medicine, Japan.

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First Department of Medicine, Osaka University School of Medicine, Japan.

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First Department of Medicine, Osaka University School of Medicine, Japan.

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First Department of Medicine, Osaka University School of Medicine, Japan.

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First Department of Medicine, Osaka University School of Medicine, Japan.

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First Department of Medicine, Osaka University School of Medicine, Japan.

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First Department of Medicine, Osaka University School of Medicine, Japan.

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First Department of Medicine, Osaka University School of Medicine, Japan.

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Published May 1, 1994 - More info

Published in Volume 93, Issue 5 on May 1, 1994
J Clin Invest. 1994;93(5):2197–2205. https://doi.org/10.1172/JCI117216.
© 1994 The American Society for Clinical Investigation
Published May 1, 1994 - Version history
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Abstract

We have reported that ischemic preconditioning may limit infarct size by increasing 5'-nucleotidase activity. The present study tested whether alpha 1-adrenoceptor stimulation in ischemic preconditioning mediates the infarct size-limiting effect through augmentation of 5'-nucleotidase activity. The coronary artery was occluded four times for 5 min separated by 5 min of reperfusion (ischemic preconditioning) in 82 dogs. Then the coronary artery was occluded for 90 min followed by 6 h of reperfusion. Infarct size normalized by risk area was smaller after ischemic preconditioning than in the control group (40.6 +/- 2.3 vs 6.7 +/- 2.0%, P < 0.001), even though no difference existed in endomyocardial collateral flow during ischemia (8.7 +/- 1.0 vs 8.9 +/- 1.0 ml/100 g per min). Ectosolic and cytosolic 5'-nucleotidase activity was increased after ischemic preconditioning. However, prazosin blunted the infarct size-limiting effect of ischemic preconditioning (infarct size: 42.8 +/- 3.7%). Intermittent alpha 1-adrenoceptor stimulation by methoxamine mimicked the increase in 5'-nucleotidase activity and the infarct size-limiting effect, which were abolished by alpha, beta,-methyleneadenosine 5'-diphosphate. Identical results were obtained in the conscious model (n = 20). Therefore, we conclude that increases in ectosolic 5'-nucleotidase activity due to alpha 1-adrenoceptor activation may contribute to the infarct size-limiting effect of ischemic preconditioning.

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