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Antecedent Ethanol Attenuates Cerebral Ischemia/Reperfusion‐Induced Leukocyte‐Endothelial Adhesive Interactions and Delayed Neuronal Death: Role of Large Conductance, Ca 2+ ‐activated K + Channels
Author(s) -
WANG QUN,
KALOGERIS THEODORE J.,
WANG MEIFANG,
JONES ALLAN W.,
KORTHUIS RONALD J.
Publication year - 2010
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2010.00041.x
Subject(s) - neuroprotection , chemistry , ischemia , potassium channel , reperfusion injury , pharmacology , intravital microscopy , hippocampus , anesthesia , apoptosis , programmed cell death , medicine , biochemistry , microcirculation
Please cite this paper as: Wang, Kalogeris, Wang, Jones and Korthuis (2010). Antecedent Ethanol Attenuates Cerebral Ischemia/Reperfusion‐Induced Leukocyte‐Endothelial Adhesive Interactions and Delayed Neuronal Death: Role of Large Conductance, Ca 2+ ‐activated K + Channels. Microcirculation 17(6), 427–438. Abstract EtOH‐PC reduces postischemic neuronal injury in response to cerebral (I/R). We examined the mechanism underlying this protective effect by determining (i) whether it was associated with a decrease in I/R‐induced leukocyte‐endothelial adhesive interactions in postcapillary venules, and (ii) whether the protective effects were mediated by activation of large conductance, calcium‐activated potassium (BK Ca ) channels. Mice were administered ethanol by gavage or treated with the BK Ca channel opener, NS1619, 24 hours prior to I/R with or without prior treatment with the BK Ca channel blocker, PX. Both CCA were occluded for 20 minutes followed by two and three hours of reperfusion, and rolling (LR) and adherent (LA) leukocytes were quantified in pial venules using intravital microscopy. The extent of DND, apoptosis and glial activation in hippocampus were assessed four days after I/R. Compared with sham, I/R elicited increases in LR and LA in pial venules and DND and apoptosis as well as glial activation in the hippocampus. These effects were attenuated by EtOH‐PC or antecedent NS1619 administration, and this protection was reversed by prior treatment with PX. Our results support a role for BK Ca channel activation in the neuroprotective effects of EtOH‐PC in cerebral I/R.