Activity of lysosomal apparatus in rat myocardium during experimental coronary and noncoronary myocardial damage.

Cardiac and plasma activities of marker lysosomal enzymes were studied in Wistar rats with metabolic (epinephrine) and occlusion (ligation of coronary arteries) myocardial infarction. Activity of all examined lysosomal enzymes significantly increased in the myocardium and blood plasma starting from the first day after ligation of the coronary arteries and was accompanied by leukocytic infiltration of the myocardium. Enzyme activity gradually decreased to postoperation day 14. In metabolic infarction leukocytic infiltration and specific activity of lysosomal enzymes rose gradually and attained maximum to postoperation day 14, while the signs of labilization of lysosomal membranes appeared from the first postoperation day. Plasma activity of lysosomal enzymes in metabolic infarction increased smoothly and peaked on day 14.

Mononuclear phagocyte system responsiveness in CCl4-induced liver cirrhosis.

In rats with CCl4-induced liver cirrhosis, a twofold decrease of blood clearance rate and a fourfold reduction in number of Kupffer cells taking up colloidal carbon particles has been demonstrated. Zymosan stimulation does not lead to granuloma-like structures in the liver of CCl4-cirrhotic rats. In cirrhotic rats, unlike controls, the cathepsin D activity of liver tissue is very little increased by zymosan treatment and there is virtually no increase in collagenolytic activity. The increase in PGE content in cirrhotic rat liver after prodigiosan stimulation was 2.5 times less than in stimulated control animals. In cirrhotic rats, the IL-1 producing capacity of blood monocytes in vitro in response to lipopolysaccharide drops almost fivefold. The total count of bone marrow-derived myeloid colonies in cirrhotic zymosan-stimulated animals was reduced by 1.5-fold whereas in control animals zymosan induced a 1.8-fold increase in the number of myeloid colonies. The number, uptake and nitroblue tetrazolium-reducing capacities of lung, spleen, peritoneal and bone marrow macrophages in animals with liver cirrhosis were only slightly increased in response to zymosan as compared to control animals. The low response of extrahepatic macrophages to stimuli in cirrhotic animals is thought to be due to their premobilization during the development of cirrhosis.

Lysosomal enzyme activity in hepatocytes and Kupffer cells from intact and partially hepatectomized rats.

Using hepatectomized rats it was shown that immediately after partial liver removal (PLR) the Kupffer macrophages were accumulated in liver remnant. At the maximal mitotic activity (36 hours following PLR) the relative amount of Kupffer cells keeps low, but 72 hours later turns out to be higher again. The periodic changes of the Kupffer cell amount in hepatectomized rats are accompanied by remarkable increase (1.5-3 fold) of free and total lysosomal enzyme activity (acid DNA-ase, acid RNA-ase, cathepsin D). The activation of the Kupffer macrophage lysosomes goes ahead of labilization of hepatocyte lysosomal membranes. The blockade of mononuclear phagocyte system by means of carbonate iron overloading in the early prereplicative period leads to an as long as 10-12 hours retardation of hepatocyte proliferation. The role of Kupffer macrophages in reparative liver regeneration is discussed.

Effect of membranous structures of the Kupffer cells on blood clotting.

The effect of subcellular fractions of the endothelia kupffer cells on blood clotting was studied. Cells were obtained from the rabbit liver by magnetic fractionation and the subcellular structures were than isolated from them by differential centrifugation. The inner membranous structures were found to carry thromboplastic activity. No correlation was found between the blood-clotting potential of the intracellular structures of the endothelial cells and the level of their cathepsin C activity.