HYPERCOAGULABLE STATE IN A HYPOBARIC, HYPOXIC ENVIRONMENT CAUSES NON-BACTERIAL THROMBOTIC ENDOCARDITIS IN RATS

HYPERCOAGULABLE STATE IN A HYPOBARIC, HYPOXIC ENVIRONMENT CAUSES NON-BACTERIAL THROMBOTIC ENDOCARDITIS IN RATS

HYPERCOAGULABLE STATE IN A HYPOBARIC, HYPOXIC ENVIRONMENT CAUSES NON-BACTERIAL THROMBOTIC ENDOCARDITIS IN RATS

Abstract

High-altitude hypoxia causes polycythaemia and a hypercoagulable state in humans and animals. This study examines the effects of a hypobaric,hypoxic environment (HHE) on the blood coagulation system in rats. A total of 170 male Wistar rats were housed in a chamber at the equivalent of 5500 m in altitude for 1-12 weeks. After 2 weeks of exposure to HHE, platelet counts decreased significantly; after 4 weeks, the prothrombin and activated partial thromboplastin times were significantly prolonged, compared with those of control rats. In addition, individual coagulation factors (VII, IX, X, XI, and XII) were significantly decreased at 8 weeks (P < 0.05). Levels of anti-thrombin III and alpha 2-plasmin inhibitor also decreased (between 4 and 8 weeks). After 4-12 weeks of exposure to HHE, 30 of 56 rats (54 per cent) developed (i) non-bacterial thrombotic endocarditis (NBTE) or (ii) infarction of the myocardium or kidney, or both (i) and (ii). The incidence of NBTE increased from 33 per cent (5/15 rats) at 4 weeks to 100 per cent (7/7 rats) at 12 weeks. Electron microscopy showed detached endothelial cells in the mitral valves at 1 week; platelets adhered to the subendocardial matrix and platelet aggregation with thrombus formation was seen at 2 weeks of exposure. The results suggest that exposure to HHE induces ahypercoagulable state and causes an NBTE in rats that may result in consumption coagulopathy.

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