Alkalosis
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Research results from P.S. Pagel and colleagues update understanding of cardioprotection
2009 MAY 11 - (NewsRx.com) -- "Intracellular acidosis during early reperfusion after coronary artery occlusion was recently linked to cardioprotection resulting from myocardial ischemic postconditioning. We tested the hypotheses that transient alkalosis during early reperfusion abolishes helium preconditioning and that the mitochondrial permeability transition pore inhibitor cyclosporin A (CsA) restores the cardioprotective effects of helium during alkalosis in vivo," scientists in the United States report. "Rabbits (n = 36) instrumented for hemodynamics measurement were subjected to a 30-min left anterior descending coronary artery occlusion and 3-h reperfusion. The rabbits received 0.9% saline (control) or three cycles of 70% helium-30% oxygen administered for 5 min interspersed with 5 min of an air-oxygen mixture before left anterior descending coronary artery occlusion in the absence or presence of transient alkalosis (pH = 7.5) produced by administration of IV sodium bicarbonate (10 mEq) 2 min before reperfusion. Other rabbits preconditioned with helium received CsA (5 mg/kg) in the presence of alkalosis or CsA alone. Helium reduced myocardial infarct size (25% +/- 4% of left ventricular area at risk; P< 0.05) compared with control (44% +/- 6%). Alkalosis during early reperfusion did not alter infarct size alone (46% +/- 2%), but this intervention abolished helium-induced cardioprotection (45% +/- 3%). CsA restored reductions in infarct size produced by helium preconditioning in the presence of alkalosis (28% +/- 6%; P< 0.05 versus control) but did not affect myocardial necrosis alone (43% +/- 6%). The results demonstrate that transient alkalosis during early reperfusion abolishes helium preconditioning in rabbits," wrote P.S. Pagel and colleagues. The researchers concluded: "CsA restored helium-induced cardioprotection during alkalosis, suggesting that helium preconditioning inhibits mitochondrial permeability transition pore formation by maintaining intracellular acidosis during early reperfusion." Pagel and colleagues published their study in Anesthesia and Analgesia (Transient Metabolic Alkalosis During Early Reperfusion Abolishes Helium Preconditioning Against Myocardial Infarction: Restoration of Cardioprotection by Cyclosporin A in Rabbits. Anesthesia and Analgesia, 2009;108(4):1076-1082). For additional information, contact P.S. Pagel, Clement J Zablocki Vet. Affairs Med Center, Anesthesia Service, 5000 W National Avenue, Milwaukee, WI 53295, USA. The publisher's contact information for the journal Anesthesia and Analgesia is: Lippincott Williams & Wilkins, 530 Walnut St., Philadelphia, PA 19106-3621, USA. Keywords: United States, Milwaukee, Acidosis, Alkalosis, Anesthesia, Blood Transfusion, Cardiology, Cardioprotection, Coronary Artery, Cyclosporin A, Drugs, Heart Attack, Medical Device, Myocardial Infarction, Pain Medicine, Perfusion, Pharmaceuticals, Reperfusion, Sodium Bicarbonate, Therapy, Transfusion Medicine, Treatment. This article was prepared by Pain & Central Nervous System Week editors from staff and other reports. Copyright 2009, Pain & Central Nervous System Week via NewsRx.com.
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