AJP - Heart and Circulatory Physiology, Vol 272, Issue 2 688-H694, Copyright © 1997 by American Physiological Society

ARTICLES

K(ATP)-channel inhibition improves hemodynamics and cellular energetics in hemorrhagic shock

A. L. Salzman, A. Vromen, A. Denenberg and C. Szabo
Division of Critical Care, Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.

We tested whether activation of K(ATP) channels contributes to vasodilatation and end-organ hypoperfusion in severe hemorrhagic shock (HS). Anesthetized juvenile pigs were hemorrhaged to a portal blood flow of 45% of baseline for 45 min and then resuscitated with Ringer lactate (RL; 100% volume of shed blood; n = 10) or RL in combination with the K(ATP)-channel antagonist glibenclamide (10 mg/kg iv bolus injection; n = 10). Addition of glibenclamide to the resuscitation fluid caused a sustained recovery of systemic blood pressure, cardiac index, portal blood flow, renal blood flow, renal cortical ATP concentration, and ileal mucosal P(CO2). Treatment with RL alone caused only a partial and transient hemodynamic and metabolic benefit. Glibenclamide treatment of sham-shocked control pigs (n = 6) transiently increased mesenteric and systemic vascular resistance. Inhibition of K(ATP)-channel activity in HS, which effectively and safely restores systemic hemodynamics, regional perfusion, and tissue metabolism, is a potentially novel therapeutic approach to the management of severe HS.

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