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1 Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana, United States; First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan
2 Medical Pharmacology and Physiology and the Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, United States; Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana, United States; First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan
3 Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana, United States
4 Medical Pharmacology and Physiology and the Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, United States
5 First Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan
6 Medical Pharmacology and Physiology and the Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, United States; Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana, United States
* To whom correspondence should be addressed. E-mail: korthuisr{at}health.missouri.edu.
Ingestion of low levels of ethanol 24 hrs prior to (ethanol preconditioning, EPC) ischemia and reperfusion (I/R) prevents postischemic leukocyte rolling (LR) and adhesion (LA), effects that were abolished by adenosine A2 receptor (ADO-A2R) antagonists or nitric oxide synthase (NOS) inhibitors. The aims of this study were to determine whether nitric oxide (NO) derived from endothelial NOS (eNOS) during the period of ethanol exposure triggered entrance into this preconditioned state and whether these events were initiated by an ADO-A2R-dependent mechanism. Ethanol or distilled water vehicle was administered to C57BL/6 (WT) or eNOS-deficient (eNOS-/-) mice by gavage. 24 hrs later, the superior mesenteric artery was occluded for 45 min. LR and LA were quantified by intravital microscopy after 30 and 60 min of reperfusion. I/R increased in LR and LA in WT mice, effects that were abolished by EPC or NO donor preconditioning (NO-PC). NO-PC was not attenuated by coincident administration of an ADO-A2R antagonist. I/R increased LR and LA in eNOS-/- mice to levels comparable to that noted in WT animals. However, EPC only slightly attenuated postischemic LR and LA, while NO-PC remained effective as a preconditioning stimulus in eNOS-/- mice. Preconditioning with an ADO-A2R agonist (which we previously demonstrated prevents I/R-induced LR and LA in WT animals) failed to attenuate these postischemic adhesive responses in eNOS-/- mice. Our results indicate that EPC is triggered by NO formed secondary to adenosine A2 receptor-dependent eNOS activation during the period of ethanol exposure 24 hrs prior to I/R.
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  M. Yusof, K. Kamada, T. Kalogeris, F. S. Gaskin, and R. J. Korthuis Hydrogen sulfide triggers late-phase preconditioning in postischemic small intestine by an NO- and p38 MAPK-dependent mechanism Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H868 - H876. [Abstract] [Full Text] [PDF]
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