KATP-channel inhibition improves hemodynamics and cellular energetics in hemorrhagic shock

Andrew L. Salzman, Amos Vromen, Alvin Denenberg, Csaba Szabo

Research output: Contribution to journalArticle

63 Scopus citations


We tested whether activation of KATP 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 KATP-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 PCO2. 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 KATP-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.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number2
StatePublished - Feb 1997
Externally publishedYes



  • Adenosine 5′-triphosphate-sensitive potassium channel
  • Glibenclamide
  • Resuscitation

ASJC Scopus subject areas

  • Physiology

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