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

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

    Research output: Contribution to journalArticle

    63 Scopus citations

    Abstract

    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 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 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.

    Original languageEnglish (US)
    Pages (from-to)H688-H694
    JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
    Volume272
    Issue number2 41-2
    StatePublished - Feb 1 1997

    Keywords

    • adenosine 5'-triphosphate-sensitive potassium channel
    • glibenclamide
    • resuscitation

    ASJC Scopus subject areas

    • Physiology
    • Cardiology and Cardiovascular Medicine
    • Physiology (medical)

    Fingerprint Dive into the research topics of 'K(ATP)-channel inhibition improves hemodynamics and cellular energetics in hemorrhagic shock'. Together they form a unique fingerprint.

  • Cite this