Cardiovascular protection of activating KATP channel during ischemia-reperfusion acidosis

Shock
Cheng-Yuan HsuYu-Chuan Tsai

Abstract

In clinical practice, prolonged occlusion of main arteries causes accumulation of metabolic waste and lactate. Reperfusion of blood flow is usually accompanied by circulatory shock. This study investigates the molecular mechanisms responsible for acidosis-induced hypotension and proposes therapeutic strategies for improving hemodynamic stability following ischemia-reperfusion acidosis. Vasomotor function of aortic rings was studied after cumulative addition of HCl in organ chambers (pH 7.4-7.0). Cultured vascular smooth muscle cells (VSMCs) were exposed to acidic buffer, and intracellular Ca levels were determined with Fluo3-AM. In an in vivo experiment, rat aorta was cross-clamped for 45 min and followed by declamping. Hemodynamic changes were measured in the presence and absence of an ATP-sensitive K channel (KATP channel) antagonist PNU37883A (3 mg/kg). Acidosis induced vasorelaxation in a dose-dependent manner, which was significantly attenuated by a KATP antagonist glibenclamide. Inhibition of KATP channel increased intracellular Ca load in the cultured VSMCs. Pretreatment with PNU37883A significantly attenuated systemic hypotension following reperfusion. However, systemic antagonism of KATP channel significantly increased...Continue Reading

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Citations

Oct 28, 2014·Medicinal Research Reviews·L TestaiV Calderone

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