Sokrut V N, Iabluchanskiĭ N I
Kardiologiia. 1991 Nov;31(11):72-5.
Myocardial infarction was simulated in experiments with 138 dogs showing normal, high, and low responses. The kinetics of creatine kinase as a marker of necrotic processes in myocardial infarction was shown to accelerate with hyperreactivity and to slow down with hyporeactivity. The kinetics of ů-glutamyl transpeptidase as a marker of reparative processes in myocardial infarction was characterized by delayed and slower evolution in hyper- and hyporeactivity. The kinetics of dienic conjugates, cyclic nucleotides (cAMP, cGMP) and immunoreactive insulin was also determined largely by the body's reactivity and the types of experimental myocardial infarction healing and was closely related to that of enzymatic markers of necrotic processes.
在138只反应正常、反应亢进和反应低下的犬类实验中模拟了心肌梗死。结果显示,作为心肌梗死坏死过程标志物的肌酸激酶动力学在反应亢进时加速,在反应低下时减慢。作为心肌梗死修复过程标志物的γ-谷氨酰转肽酶动力学在反应亢进和反应低下时表现为延迟和缓慢演变。二烯共轭物、环核苷酸(cAMP、cGMP)和免疫反应性胰岛素的动力学也在很大程度上取决于机体的反应性以及实验性心肌梗死愈合的类型,并且与坏死过程的酶标志物密切相关。