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- W4210794115 abstract "We recently demonstrated that preconditioning with an exogenous hydrogen sulfide (H2S) donor (NaHS-PC) 24 h prior to ischemia and reperfusion (I/R) causes postcapillary venules to shift to an anti-inflammatory phenotype in C57Bl/6 wild-type mice such that these vessels fail to support leukocyte rolling (LR) and leukocyte adhesion (LA) during reperfusion. The objective of the present study was to determine whether the calcium-sensitive large conductance K channel (BKCa channel) is also involved as an initiator of the anti-inflammatory phenotype elicited by H2S. The postischemic anti-inflammatory effects of NaHS-PC were abolished by BKCa channel inhibitor treatment (paxilline) when administered coincident with NaHS, 24 hrs prior to I/R. Moreover, preconditioning with the BKCa channel activator, NS-1619, was as effective as NaHS-PC in preventing I/R-induced leukocyte rolling and adhesion. Our data is consistent with the concept that H2S induces the development of an anti-adhesive state in I/R by a BKCa channel-dependent mechanism. (Patch-clamp studies are presented separately). Supported by AA14945, DK43785 and HL71796" @default.
- W4210794115 created "2022-02-08" @default.
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- W4210794115 date "2008-03-01" @default.
- W4210794115 modified "2023-10-16" @default.
- W4210794115 title "ANTECEDENT HYDROGEN SULFIDE ELICITS AN ANTI‐INFLAMMATORY PHENOTYPE IN POSTISCHEMIC MURINE SMALL INTESTINE: ROLE OF BK Ca CHANNEL" @default.
- W4210794115 doi "https://doi.org/10.1096/fasebj.22.1_supplement.730.37" @default.
- W4210794115 hasPublicationYear "2008" @default.
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