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  • Title: [Altitude exposure induces hypoxic preconditioning of the heart].
    Author: Tanaka S, Karck M, Steinhoff G, Haverich A.
    Journal: Langenbecks Arch Chir Suppl Kongressbd; 1998; 115(Suppl I):669-74. PubMed ID: 14518339.
    Abstract:
    Under in vitro conditions, the resistance to ischemia may be improved by hypoxic preconditioning. This study was designed to test the hypothesis, that hypoxic preconditioning can also be induced in vivo by exposure of an intact animal to simulated high altitude. Male Wister rats (n = 48) were exposed for 60 minutes to simulated high altitude at 3000 m or 5000 m above sea level in a hypobaric chamber. 30, 150 or 300 min following exposure, hearts were excised and perfused aerobically in the working heart model prior to 45 minutes of global ischemia at 30 degrees C and subsequent normothermic reperfusion. For control, hearts of unexposed rats were either preconditioned by one cycle of 5 minutes of normothermic ischemia and reperfusion prior to subsequent ischemia or (n = 8) or not (n = 8). Postischemic measurements included functional parameters such as aortic flow, maximum developed left ventricular pressure, creatine kinase leakage from collected samples of the coronary effluent and the morphometric assessment of the area of myocardium at risk. When compared to non-preconditioning, ischemic preconditioning significantly improved the recovery of aortic flow, left ventricular systolic pressure and reduced the postischemic creatine kinase leakage. Likewise, exposure to a simulated high altitude at 3000 m above sea level significantly improved the recovery of aortic flow and reduced creatinkinase leakage when the time interval between exposure to simulated high altitude and perfusion was set to 150 minutes. Further increase in hypoxic stress (5000 m above sea level) or the reduction of this time interval to 30 minutes reduced postischemic recovery of hearts. The exposure of an intact organism to simulated high altitude can improve the resistance of the heart to ischemia by hypoxic preconditioning. The induction of this beneficial effect depends on the level of hypoxic stress and the time interval between preconditioning and subsequent ischemia.
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