Trofymova I M, Dosenko V Ie, Byts' Iu V
A. A. Bogomoletz National Medical University, Kiev.
Fiziol Zh (1994). 2001;47(6):24-9.
In modeling of different types of acidosis (hyperchloraemic, lactate and ketoacidosis in the starvation) at rats the elastase activity, contents of alpha-2 macroglobulin (alpha 2M) and alpha-1 proteinase inhibitor (alpha 1PI) in aorta tissues and blood serum were studied. The obtained results indicate that the degree of disturbance in system elastase-inhibitors depends on expressiveness of parameters changes in system of acid-base state regulation. In modeling of various types of acidosis coefficient inhibitors/elastase is reduced due to different parameters change in aorta, namely decrease of alpha 2M contents--in hyperchloraemic acidosis, increase of elastase activity--in lactat-acidosis, increase of elastase activity and decrease of alpha 2M contents--in ketoacidosis. In blood serum the similar coefficient is reduced due to increase of elastase activity and decrease of alpha 2M contents in hyperchloraemic acidosis and starvation, and, in turn, due to decrease of alpha 2M contents--in lactat-acidosis. The obtained data indicate that one of mechanisms of vascular wall damage in acidosis is disturbance of balance between elastase and its inhibitors in tissues of arteries.
在对大鼠不同类型酸中毒（高氯性酸中毒、饥饿性乳酸酸中毒和酮症酸中毒）进行建模时，研究了主动脉组织和血清中弹性蛋白酶活性、α-2巨球蛋白（α2M）和α-1蛋白酶抑制剂（α1PI）的含量。所得结果表明，弹性蛋白酶-抑制剂系统的紊乱程度取决于酸碱状态调节系统中参数变化的表现程度。在各种类型酸中毒的建模中，抑制剂/弹性蛋白酶系数降低，原因是主动脉中不同参数发生变化，即高氯性酸中毒时α2M含量降低，乳酸酸中毒时弹性蛋白酶活性增加，酮症酸中毒时弹性蛋白酶活性增加且α2M含量降低。在血清中，高氯性酸中毒和饥饿时，由于弹性蛋白酶活性增加和α2M含量降低，该系数降低，而在乳酸酸中毒时，则是由于α2M含量降低导致该系数降低。所得数据表明，酸中毒时血管壁损伤的机制之一是动脉组织中弹性蛋白酶与其抑制剂之间的平衡受到干扰。
