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AICAR preconditioning prevents postischemic leukocyte rolling and adhesion: role of K(ATP) channels and heme
F Spencer Gaskin1, Kazuhiro Kamada, Mozow Yusof
1Department of Medical Pharmacology and Physiology, University of Missouri-Columbia, One Hospital Drive, Columbia, MO 65212, USA.
Objective:
We previously demonstrated that pharmacologic activation of AMP-activated protein kinase (AMPK) with 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside (AICAR) 24 hours prior to (AICAR preconditioning; AICAR-PC) ischemia/reperfusion (I/R) prevents postischemic leukocyte-endothelial cell adhesive interactions (LEI) by a mechanism initiated by endothelial nitric oxide synthase (eNOS)-dependent NO production during the period of AICAR-PC. The major aim of this study was to examine the role of ATP-sensitive potassium (K(ATP)) channels and heme oxygenase as mediators of the antiadhesive effects of AICAR-PC during I/R 24 hours later.
Methods:
Intravital fluorescence microscopy was used to quantify LEI in the small intestine of AICAR-preconditioned C57BL/6J mice treated with K(ATP) channel or heme oxygenase inhibitors during I/R 24 hours after AICAR-PC in separate experiments.
Results:
I/R induced marked increases in LEI relative to sham control mice, proadhesive responses that were prevented by AICAR-PC 24 hours prior to I/R. The effects of AICAR-PC to prevent postischemic LEI were abolished by K(ATP) channel or heme oxygenase inhibition during I/R.
Discussion/Conclusion:
Our results indicate that the antiadhesive effects of AICAR-PC are mediated by K(ATP) channel- and heme oxygenase-dependent mechanisms during I/R.
