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Wiley, British Journal of Pharmacology, 1(140), p. 91-96, 2003

DOI: 10.1038/sj.bjp.0705406

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Dexamethasone improves vascular hyporeactivity induced by LPS in vivo by modulating ATP‐sensitive potassium channels activity

This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

Septic shock represents an important risk factor for patients critically ill. This pathology has been largely demonstrated to be a result of a myriad of events. Glucocorticoids represent the main pharmacological therapy used in this pathology.Previously we showed that ATP-sensitive potassium (KATP) channels are involved in delayed vascular hyporeactivity in rats (24 h after Escherichia coli lipopolysaccharide (LPS) injection). In LPS-treated rats, we observed a significant hyporeactivity to phenylephrine (PE) that was reverted by glybenclamide (GLB), and a significant increase in cromakalim (CRK)-induced hypotension.We evaluated the effect of dexamethasone (DEX 8 mg kg−1 i.p.) whether on hyporeactivity to PE or on hyperreactivity to CRK administration, in vivo, in a model of LPS (8 × 106 U kg−1 i.p.)-induced endotoxemia in urethane-anaesthetised rats.DEX treatment significantly reduced, in a time-dependent manner, the increased hypotensive effect induced by CRK in LPS-treated rats. This effect was significantly (P