Abstract
Platelets have been known to be an important factor in thrombogenesis. In an early stage of thrombosis, platelets adhere to exposed subendothelial collagen eliciting release of ADP and aggregate each other. ADP seems to be a very important substance in platelet thrombosis. In this experiment ADP was injected into the vein in 7 control Wistar rats and 6 spontaneously hypertensive rats (SHR). SHR were administered with 0.1% NaCl as drinking water over a period of 10 weeks and the blood pressure showed to be 200mmHg or above.
ADP 1mg/kg was injected rapidly into the jugular vein of the anesthetized rats. Blood samples were collected from carotid cannula before and 30sec, 3, 10, 20 and 30min after the injection. EKG and respiration were monitered and recorded continuously. 51Cr-labeled platelets were infused in 2 rats. They were sacrificed 1min after ADP injection and the organs were studied for the radioactivity and the histological observation. In control animals, platelet count decreased immediately after the ADP injection. Variable A-V block, premature beats and apnea developed immediately after the injection and subsided by 1min. Arterial hypotension and rise in the central venous pressure were also observed for a period of 10min and gradually subsided. In the analysis of platelet radioactivity, platelets were revealed to accummulate unproportionally in the lungs. Histological examination revealed platelet thrombi in the pulmonary microvas-culature.
In SHR rats, decrease in platelet count and heart rate, degree of arrhythmia, apnea, systemic hypotension and elevation in central venous pressure after ADP injection were less than in control rats. In the platelet volume study, the mode related volume was at 2.7μ3 in SHRs as compared with the mode of 2.4μ3 in controls. The volume distribution curve in SHR shifted to the left indicating a relative increase in smaller platelets in the population.
In summery, ADP injected into the central vein produced platelet aggregation which were trapped in the pulmonary microvasculature causing pulmonary thromboembolism. Arrhythmia and respiratory distress seems to be due to transient pulmonary thromboembolism. These changes were less severe in SHRs. These results would suggest that hypertension and/or possible association of the vascular change cause different attitude of platelets to ADP.
