According to current concepts, pathogenesis of intravascular trombus formation is underlaid by three crucial factors: lesion of the vascular wall, impairment of hemodynamics and hemostatic properties of the blood. While admitting the important role of each of these factors, one should acknowledge that the true nature of thrombosis is much more complicated and does not always fit the framework of this triad. In our experiments on rabbits, it was demonstrated that the thrombotic process in the basin of the pulmonary vessels could be successfully reproduced even in intact animals under conditions of disturbed immune homeostasis. A distinctive feature of immune thrombosis of the pulmonary vessels was a generalized lesion of the microcirculatory bed, gradual increase in the thrombotic masses and involvement of the major branches of the pulmonary vessels (PV). Morphologically, a picture of lymphoid-cellular infiltration and localization of the antigenic complex in the affected PV was revealed. As a result of progressive decrease in the pulmonary arterial blood circulation and increasing resistance in the system of the lesser circulation there were noted, already during the first hours after the onset of the capillary thrombosis, a compensatory hyperfunction of the right ventricle of the heart which was manifested in its highly increased contractility, higher levels of cyclic AMP and phosphorylation potential. At a later period, however, the compensatory possibilities of the right ventricle of the heart failed to overcome this resistance with resulting incompetence of the organ starting to develop within 2-3 days.
The Role of G Protein-Coupled Receptors in the Right Ventricle in Pulmonary Hypertension
