Hemodynamic effects of @entity5217 during XXXX : contrasting findings in vitro versus in vivo.

@entity5694 @entity326 @entity235 @entity526 @entity5217 @entity26 @entity842 @entity35 @entity1063 @entity855
The final common pathway involved in the cardiovascular alterations of @entity326 is incompletely defined. The opening of KATP channels is associated with vasorelaxation and alterations in cardiac contractility. This event may be triggered during @entity326 by increased @entity842 (NO) production, by a decreased intracellular content of @entity855 , or by a change in the transmembrane electrical potential. In the present study, we assessed the effects of @entity5217 , an agent that blocks the opening of KATP channels in vitro, on the contractile response of @entity35 aortic rings to @entity1063 , and in vivo in anesthetized @entity235 , with or without exposure to @entity526 endotoxin. In vitro, @entity5217 decreased the contractile response to @entity1063 in the presence of endotoxin, provided that the endothelium was intact. In vivo, administration of 0.15 mg/kg increased systemic vascular resistance (SVR) in the absence of endotoxin only, and increased myocardial performance. A higher dose of 1 mg/kg increased SVR and decreased myocardial performance, both during @entity326 and in control conditions. Renal and mesenteric blood flows decreased, but the respective fractional flows were unchanged. @entity26 delivery decreased in both experimental conditions, but @entity26 consumption decreased only in control conditions. The in vitro observations suggest that the opening of KATP channels is involved in the regulation of vascular tone during @entity5694 , via an endothelium-dependent mechanism. As different effects of @entity5217 were observed in vivo, the importance of the opening of KATP channels in @entity326 may be limited.
