Ravingerová T, Styk J, Ziegelhöffer A, Slezák J, Tribulová N, Pissarek M
Institute for Heart Research, Slovak Academy of Sciences, Bratislava.
Bratisl Lek Listy. 1991 Feb;92(2):102-7.
The role of ischemia itself, calcium overload and of reactive oxygen species (ROC) in reperfusion injury of the heart was characterized from the physiological, biochemical and morphological point of view. Experiments were performed on isolated rat hearts (Langndorff preparation), perfused at constant pressure of 65 Torr and 37 degrees C. The effect of ischemia was studied on the model of 30 min normothermic global ischemia with consequent 30 min reperfusion. Calcium overload and damage by ROS were modelled by Ca(2+)-paradox (3 min Ca(2+)-depletion followed by 10 min Ca(2+)-repletion) and by intraaortal bolus application of ROS-generating system (H2O2 + FeSO4) respectively. Evaluation of functional and biochemical parameters revealed that the changes in electrical activity, accumulation of lactate and the loss in total adenine nucleotides content in heart tissue may be well applied to characterize the participation of the above mechanisms on total reperfusion damage to the heart. Histochemically detected different patterns of distribution of enzyme activities also allow to distinguish between alterations caused by different factors of reperfusion injury.
从生理、生化和形态学角度对缺血本身、钙超载及活性氧（ROC）在心脏再灌注损伤中的作用进行了表征。实验在离体大鼠心脏（Langndorff 制备）上进行，在 65 托恒定压力和 37℃下灌注。研究了在 30 分钟常温全心缺血随后 30 分钟再灌注模型上的缺血作用。分别通过钙反常（3 分钟钙耗竭随后 10 分钟钙再充盈）和主动脉内推注活性氧生成系统（H2O2 + FeSO4）模拟钙超载和活性氧损伤。对功能和生化参数的评估表明，心脏组织电活动的变化、乳酸的积累以及总腺嘌呤核苷酸含量的损失可很好地用于表征上述机制对心脏再灌注总损伤的参与情况。组织化学检测到的酶活性分布的不同模式也有助于区分由再灌注损伤的不同因素引起的改变。
