Tribulová N, Slezák J, Ravingerová T, Styk J, Gabauer I
Ustavu pre výskum srdca SAV, Bratislave.
Bratisl Lek Listy. 1991 Feb;92(2):81-90.
The fine structural alteration and histochemical changes of the cardiac conduction system were studied in dogs and rats using various models of ischemic and reperfusion injury. The role of Ca2+ overload and reactive oxygen species (ROS) per se were also investigated. In all models of injury the activity of glycogen phosphorylase (histochemical indicator of the early ischemic changes) was present in nodal and conducting cells, although it was markedly diminished or absent in surrounding contractile muscle. Fine structural ischemic alterations progressed more slowly in conducting cells in comparison with working myocardial cells. Changes induced by Ca2+ paradox or ROS were reversible in conducting tissue in contrast to working myocardial tissue. The observations support the concept that conducting cells are more resistant to ischemia and also to reperfusion related injury than contractile myocardial cells.
利用各种缺血和再灌注损伤模型，对犬和大鼠心脏传导系统的精细结构改变和组织化学变化进行了研究。同时还研究了钙离子超载和活性氧本身的作用。在所有损伤模型中，糖原磷酸化酶的活性（早期缺血变化的组织化学指标）在结细胞和传导细胞中存在，尽管在周围收缩肌中明显减弱或不存在。与工作心肌细胞相比，传导细胞的精细结构缺血改变进展较慢。与工作心肌组织相比，钙离子反常或活性氧诱导的变化在传导组织中是可逆的。这些观察结果支持这样一种观点，即传导细胞比收缩性心肌细胞对缺血以及再灌注相关损伤更具抵抗力。
