Changes of coagulation and fat-metabolism following pulmonary microembolism after trauma and hemorrhage.

In 16 of 24 anesthetized mongrel dogs a standardized bone trauma was performed to both hind legs by open osteootmy. During the following 6 hours the most important hemodynamic parameters, total platelet count (GTZ) and its separate fractions (NKF, KF) were continously monitored. Five hours after the trauma 50% of the total blood volume (taken to be 80 ml/kg body weight) was withdrawn from two of the four groups of animals. The trauma caused no direct effect on the pulmonary hemodynamics. In the following hours there was a slight decrease of cardiac output (HZV) in the traumatised animals. Besides a moderate increase in mean pulmonary pressure (MPP), pulmonary vascular resistance (PVR) increased by 72% of the pretraumatic values. The application of intravascular catheters diminished the total platelet count markedly in the injured, as in the uninjured animals. The increase in PVR was caused less by a mechanical obstruction of the pulmonary capillary bed than by vasoactive substances released by the platelets. The following hemorrhage led to a more marked hemodynamic reaction in the injured animals. All these animals died before the end of the calculated hemorrhage. All animals without trauma survived. Irreversible aggregation of platelets developed in the pulmonary capillary bed caused by the marked pulmonary hypocirculation. Histological examination showed a marked disseminated pulmonary microthrombosis in all animals with trauma and hemorrhage. The initial phase of experimental pulmonary microembolism caused by trauma was characterized by pulmonary hypocirculation and an activated coagulation with simultaneously diminished total platelet count.