Reduced tolerance to reperfusion-associated injury in hearts from myopathic hamsters.
This study was done to evaluate the response of myopathic hearts from dystrophic hamsters to 30 minutes of ischemia followed by 30 minutes of reperfusion. Hearts from male and female normal animals recovered 77 +/- 6% and 64 +/- 5% of their contractile force respectively following reperfusion whereas only 34 +/- 8% (male) and 34 +/- 7% (female) recovery was seen in myopathic hearts (P less than 0.01). Substantial sustained contractures were observed during reperfusion in hearts from dystrophic animals irrespective of gender whereas none were seen with control hearts. Reperfusion produced a rapid release of CPK that peaked at 5 minutes (approximate coronary effluent concentration of 40 mU/ml) and remained elevated for the reperfusion duration. Peak CPK values for normal hearts were reached at 10 minutes following reperfusion, were significantly lower from the myopathic hearts and returned to near control levels at the end of the 30 minute reperfusion period. Reducing Ca2+ in the perfusion medium by up to 80% or perfusing the hearts with the Ca2+-channel blocker verapamil produced no beneficial effects. Changes in the above parameters produced by ischemia or heart rate alterations throughout the perfusion sequence were not different between normal and myopathic hearts. This study shows a sensitivity of myopathic hearts that is manifested during reperfusion. Possible mechanisms for this reduced tolerance are discussed.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D009202:Cardiomyopathies / Q000503:physiopathology*; D003327:Coronary Disease / Q000503:physiopathology*; D003402:Creatine Kinase / Q000378:metabolism; D006224:Cricetinae; D005260:Female; D008297:Male; D008647:Mesocricetus; D009200:Myocardial Contraction; D010477:Perfusion
D003402:Creatine Kinase; D002118:Calcium