Disorders of the system of hemostasis and biochemical parameters of NZB/NZW F1 mice
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KeywordsCollagen Animal Model Cortisol Serotonin Fibrinogen
Object of a research. A research of interaction of coagulation and biochemical parameters of NZB/NZW F1 mice with spontaneous explicating lupus like disease.
120 female mice of a line NZB/NZW F1 3 months age were investigated. Coagulation tests were used: counting platelets, activated partial thromboplastin time (APTT), throbmin time (TT), prothrombin time (PT), concentation of fibrinogen, soluble fibrin monomer complexes (SFMC); pararmeters of platelet aggregate (spontaneous and induced with ristocetin, collagen and ADF). Biochemical parameters of serotonin and cortisol were investigated. An electronic microsocopy of microvessels was investigated also.
Significant (more than twice) decreasing the amount of platelets of NZB/NZW F1 mice, elongation of parameters of the coagulation tests (APTT 40,0 ± 2,7 sec, control 27,6 ± 2,5 sec) (P < 0,01), decreasing the concentration of fibrinogen (1,1 ± 0,2 g/l, control 5,2 ± 0,6 g/l), increasing the level SFMC (28,1 × 10-2 ± 1,6 g/l, control 8,9 × 10-2 ± 1,03 g/l), increasing the parameter of spontaneous platelets aggregate (20,3 ± 1,96 %, control 2,5 ± 0,6 %) and aggregate of platelets with ADF (12,8 ± 1,3 %, control 9,0 ± 0,8 %) decreasing the aggregate with collagen (4,4 ± 0,6 %, contol 9,3 ± 0,8 %) were registered. The concentration of "plasma" serotonin was increased (0,065 mcg/ml, control 0,042 mcg/ml), the level of cortisol was considerably reduced (0,4 ± 0.09 mcg/ml, control 1,03 mcg/ml). The correlation between increasing the concentration of "plasma" serotonin, increasing the parameter of the spontaneous aggregate of platelets, increasing the concentration of SFMC, elongation of the coagulation tests and decreasing the concentration of "platelet" serotonin were marked. By the electronic microscopy the distrophy of endothelium is registered.
Thus the endothelial damage of NZB/NZW F1 mice was accompanied by the expressed activation of a system of hemostasis, amplifying the aggregate of platelets and increasing the release of serotonin from them. At the same time the significant decreasing the concentration of cortisol was found. These disorders of hemostasis are typical for DIC syndrome. Therefore, it is possible to use NZB/NZW F1 mice as an animal model for study of disorders of hemostasis, including DIC syndrome, for the patients with SLE.