The role of platelet reactivity in thrombogenesis (II)

Platelet aggregation is an important phenomenon in the first step of thrombogenesis. When platelets aggregate, ADP and other platelet aggregating and vasoactive substances may release. We reported that an injection of ADP caused pulmonary thromboembolism in rats associated with transient effects including thrombocytopenia, apnea, arrhythmia, rise in central venous pressure and fall in arterial blood pressure, while these changes were less severe in SHRs. In this study, platelet aggregability and thrombogenic tendency in response to ADP were analysed in SHRs in comparison with those in the control rats. 30 Wistar rats (control) and 30 SHRs (20-30 weeks old) were used. Blood samples were taken from carotid artery cannula for an analysis of platelet count, platelet volume and platelet aggregation by ADP. ADP (1mg/kg) was injected rapidly into the jugular vein of anesthetized rats. After ADP injection, blood samples were taken at 30sec, 3, 10, 20 and 30min. ECG and respiration were recorded continuously. Before ADP injection, platelet count (control; 53.1, SHR; 53.0×104/μl), the mode related platelet volume (control; 2.6, SHR; 2.7μ3) and platelet ADP content (control; 2.4, SHR; 2.7μmoles/1011pl.) were not different between the two groups. Maximum intensity of ADP (10μM) aggregation was significantly lower in SHR (39.4±4.8%) than in the control (50.3±5.1%) (p<0.05). After the injection, platelet count decreased to 59.7% of preinjection level at 30sec (p<0.01) and returned to 93.8% at 3min in the control; 90.5% at 30sec (p<0.01) and 74.9% at 3min in SHR. Platelet ADP content decreased to 61% at 10min in the control, while little change in SHR. Arrhythmia and apnea observed after ADP injection were significantly longer continued in the control (p<0.01). Histological study revealed that pulmonary microvasculature was frequently filled with platelet thrombi in the control and seldom in SHR. The lower incidence in pulmonary microthromboembolism in SHR might be related to its in vitro hypoaggregability of platelet due to the insufficient release reaction. The lower response of platelet might be explained by exhaustion under hypertensive stress, though further investigation is required.