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  • Title: [Pulmonary microembolism: pulmonary hemodynamics following trauma and hemorrhage (author's transl].
    Author: Ulmer HE, Saggau WW.
    Journal: Basic Res Cardiol; 1975; 70(4):406-19. PubMed ID: 1191208.
    Abstract:
    Standardized bone trauma by means of open osteotomy is performed on both hind legs of 16 out of 24 anaesthetised mongrels. During the following 6 hours the most important parameters of blood coagulation and the serum lipids are estimated at regular intervals. Subsequently in a number of the animals 50% of the total blood volume is withdrawn continuously over a period of one hour. All animals without the preceding trauma survive the hemorrhage. The animals in the trauma group die on the average 42 minutes after the beginning of the hemorrhage. The trauma causes an acute decrease in total platelet count (GTZ) to 40% of the pretraumatic value. During an initial phase of hypercoagulability there is a formation of reversible microaggregations containing platelets and fibrin, caused by an increased turnover of coagulation factors. Secondary fibrinolysis develops in the traumatised animals. A further increase in coagulation is caused by the following hemorrhage. In combination with decreased and inhibited fibrinolysis, a disseminated intravascular coagulation state is found and results in irreversible pulmonary microthrombosis. Massive pulmonary fat deposits cannot be found histologically in spite of an increase in serum triglycerid levels to 35% above the pretraumatic values. In dogs great amounts of fat are filtered by the glomeruli and are demonstrable in the tubular epithelium. Histological examinations show a marked disseminated pulmonary microthrombosis of platelets, fibrin and fat in those animals with trauma and hemorrhage. Only the accompanying hypovolemia produces the characteristic histologic changes of the so-called Pulmonary Microembolism Syndrome.
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