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A1 adenosine receptor antagonists block ischemia-reperfusion injury of the lung

A1 adenosine receptor antagonists block ischemia-reperfusion injury of the lung Neely, Constance F., and Ingegerd M. Keith. receptor antagonists block ischemia-reperfusion injury of the lung. Am. J. Physiol. 268 (Lung CeZZ. Mol. Physiol. 12): LlO36-L1046, 1995.-Ischemia-reperfusion (I-R) injury of the lung occurs after lung transplantation, pulmonary thromboembolectomy, or cardiopulmonary bypass. In the heart, adenosine, receptor agonists, and a brief period of preconditioning ischemia attenuate I-R injury. Moreover, in the lung, thromboxane is released during ischemia and is an important mediator of I-R injury. We previously reported that adenosine produces vasoconstriction in the feline pulmonary vascular bed by acting on Al receptors to induce the release of thromboxane and that these vasoconstrictor responses are desensitized by low doses of Al receptor agonists. Because Al receptor agonists mimic the effect of preconditioning ischemia, we hypothesized, in contrast to previously proposed mechanisms, that small amounts of adenosine released during preconditioning ischemia desensitize A1 receptors. Also, we hypothesized that greater amounts of adenosine are released after longer periods of ischemia, which activate Al receptors. Thus if desensitization of Al receptors is the mechanism by which preconditioning attenuates I-R injury of the heart and A1 receptor activation during ischemia plays an important role in I-R injury of the lung, Al receptor antagonists should http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Lung Cellular and Molecular Physiology The American Physiological Society

A1 adenosine receptor antagonists block ischemia-reperfusion injury of the lung

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Publisher
The American Physiological Society
Copyright
Copyright © 1995 the American Physiological Society
ISSN
1040-0605
eISSN
1522-1504
Publisher site
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Abstract

Neely, Constance F., and Ingegerd M. Keith. receptor antagonists block ischemia-reperfusion injury of the lung. Am. J. Physiol. 268 (Lung CeZZ. Mol. Physiol. 12): LlO36-L1046, 1995.-Ischemia-reperfusion (I-R) injury of the lung occurs after lung transplantation, pulmonary thromboembolectomy, or cardiopulmonary bypass. In the heart, adenosine, receptor agonists, and a brief period of preconditioning ischemia attenuate I-R injury. Moreover, in the lung, thromboxane is released during ischemia and is an important mediator of I-R injury. We previously reported that adenosine produces vasoconstriction in the feline pulmonary vascular bed by acting on Al receptors to induce the release of thromboxane and that these vasoconstrictor responses are desensitized by low doses of Al receptor agonists. Because Al receptor agonists mimic the effect of preconditioning ischemia, we hypothesized, in contrast to previously proposed mechanisms, that small amounts of adenosine released during preconditioning ischemia desensitize A1 receptors. Also, we hypothesized that greater amounts of adenosine are released after longer periods of ischemia, which activate Al receptors. Thus if desensitization of Al receptors is the mechanism by which preconditioning attenuates I-R injury of the heart and A1 receptor activation during ischemia plays an important role in I-R injury of the lung, Al receptor antagonists should

Journal

AJP - Lung Cellular and Molecular Physiology – The American Physiological Society

Published: Jun 1, 1995

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