[Effect of acid-base imbalance on the equilibrium of elastase and its inhibitors in rat serum and aorta tissues].
In experiments on the acid-base imbalance modelling (acidosis induced with either lactate or ammonium chloride alcalosis induced with sodium hydrocarbonate) in rats, there were studied elastase activity, alpha-2-macroglobulin and alpha-1 proteinase inhibitor contents in blood serum and tissues of the aorta. The results obtained indicated that, in the models of both acidosis and alcalosis an disbalance between elastase and its inhibitors was observed. However, in NH4CL-acidosis in homogenates of aorta the inhibitors/elastase coefficient decreased at the expense of a reduction in contents of alpha-2-macroglobulin, while in lactate-acidosis it only decreased at the expense of an increase in elastase activity. In alcalosis, contents of proteinase inhibitors were even increased, however a substantial increase in elastase activity indicated a reduction in integrative coefficient. Similar changes were observed in blood serum, except elastase activity was considerably elevated in NH4CL-acidosis and did not change in lactate-acidosis. Thus, an disbalance in the elastolytic system associated with different types of acid-base imbalance can promote the destruction of elastic fibers of aorta, which is considered as one of initial mechanisms in pathogenesis of arteriosclerosis.
Trofymova
I M
IM
A.A. Bogomoletz National Medical University, Ministry of Public Health of Ukraine, Kiev.
Dosenko
V Ie
VIe
Byts'
Iu V
IuV
D000137:Acid-Base Imbalance; D000138:Acidosis / Q000378:metabolism; D000471:Alkalosis / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000201:enzymology / Q000378:metabolism*; D004195:Disease Models, Animal; D010196:Pancreatic Elastase / Q000037:antagonists & inhibitors / Q000097:blood / Q000378:metabolism*; D051381:Rats; D000515:alpha 1-Antitrypsin / Q000378:metabolism*; D000511:alpha-Macroglobulins / Q000378:metabolism
D000515:alpha 1-Antitrypsin; D000511:alpha-Macroglobulins; D010196:Pancreatic Elastase