Karmazyn M
Basic Res Cardiol. 1985 Jul-Aug;80(4):392-8. doi: 10.1007/BF01908183.
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.
本研究旨在评估营养不良仓鼠的心肌病变心脏在经历30分钟缺血和30分钟再灌注后的反应。雄性和雌性正常动物的心脏在再灌注后分别恢复了其收缩力的77±6%和64±5%，而心肌病变心脏的恢复率仅为34±8%（雄性）和34±7%（雌性）（P<0.01）。无论性别如何，在营养不良动物的心脏再灌注期间均观察到大量持续性挛缩，而对照心脏则未观察到。再灌注导致肌酸磷酸激酶（CPK）迅速释放，在5分钟时达到峰值（冠状动脉流出液浓度约为40 mU/ml），并在再灌注期间持续升高。正常心脏的CPK峰值在再灌注后10分钟达到，显著低于心肌病变心脏，在30分钟再灌注期结束时恢复到接近对照水平。将灌注培养基中的Ca2+减少多达80%或用Ca2+通道阻滞剂维拉帕米灌注心脏均未产生有益效果。在整个灌注过程中，缺血或心率改变所引起的上述参数变化在正常心脏和心肌病变心脏之间并无差异。本研究显示了心肌病变心脏在再灌注期间表现出的敏感性。文中讨论了这种耐受性降低的可能机制。
