The Role of Nitric Oxide Synthase and Heme Oxygenase in the Protective Effect of Hypothermia in Ischemia-Reperfusion Injury

• DOI: 10.2106/jbjs.h.01324
• Publication Date: 2009-11-02T18:32:43Z
• Authors: Russell Ward; Nicholas Souder; Daniel Stahl; Felicia Hunter; Robert Probe; Christopher Chaput; Ed Childs
• Keywords: Vascular permeability; Intravital microscopy

Background: Ischemia-reperfusion injury plays an important role in limb salvage following ischemia. The purpose of the present study was to evaluate effect local hypothermia and chemical modulators on microvascular permeability ischemia-reperfusion skeletal muscle. Methods: Sprague-Dawley rats were randomized into nine groups. Postcapillary venules extensor digitorum longus muscle visualized with use intravital microscopy. Following intravenous bolus fluorescein isothiocyanate-labeled albumin, intravascular extravascular space examined for leak. Rats sham group underwent a one-hour mock ischemic period without application femoral artery tourniquet, followed by one hour reperfusion. treatment groups (n = 5 each group) had tourniquet applied hour, reperfusion at 10°C (cold) alone, nitric oxide synthase inhibitor, heme oxygenase combination inhibitors, 34°C (warm) inducer, or inducers. Results: did not show significant increase permeability. warm ischemia/reperfusion displayed increases permeability, as that received inhibitors 10°C. No observed animals cold inducers 34°C. Conclusions: Local protects from increased injury. This protective is also seen induction systems physiologic temperature. We have shown effects are blocked giving while keeping hypothermic. These findings demonstrate play combined injury, suggesting possible pathways clinical intervention modulate trauma, use, vascular surgery, surgery. Clinical Relevance: provides evidence ischemia-reperfusion-related tissue biochemical insight future pharmacologic intervention.