Fetisova T V, Sokolova G G
Kardiologiia. 1979 Jan;19(1):98-102.
It was shown in dog experiments that the formation and content of the adenosine precursor in the zone of the infarction and the surrounding parts of the myocardium undergo no essential changes. At the same time, further conversion of adenosine monophosphate in an infarction heart is deeply disturbed due to shifts in the enzymatic systems of the adenosine cycle. In the area of the necrosis adenosine monophosphate is metabolized mainly without the production of adenosine because high activity of AMP aminohydrolase here occurs in conjunction with deep inhibition of 5-nucleotidase. Diametrically opposite relationships are created in the myocardium outside of the focus of infarction and adenosine production does not suffer evidently. In both areas of the involved heart adenosine decomposition is delayed due to the inhibition of adenosine deaminase, but in the infarction zone this shift is restricted to 48 hours whereas in the periinfarction zone it is not corrected even 10 days after reproduction of the pathological condition.
犬实验表明,梗死区及心肌周边部位腺苷前体的形成和含量无本质变化。与此同时,由于腺苷循环酶系统的改变,梗死心脏中一磷酸腺苷的进一步转化受到严重干扰。在坏死区域,一磷酸腺苷主要在不产生腺苷的情况下代谢,因为此处AMP氨基水解酶的高活性与5 -核苷酸酶的深度抑制同时发生。在梗死灶外的心肌中则形成了完全相反的关系,腺苷生成未明显受损。在受累心脏的两个区域,由于腺苷脱氨酶的抑制,腺苷分解均延迟,但在梗死区这种变化仅限于48小时,而在梗死周边区,即使在病理状态重现10天后仍未恢复正常。