抄録
Previously we have reported that an intravenous injection of ADP into normal Wistar rats (NWR) induced pulmonary thromboembolism, while this change was scarecely seen in spontaneously hypertensive rats (SHR) and that platelet count, volume and ADP·ATP contents were not different between SHR and NWR before the ADP injection.
In this paper, in vitro platelet function, platelet aggregation and release reaction, and in vivo ADP release reaction were analyzed. Similar study was also performed in young SHR in which hypertension had not been established to determine whether hypertension plays influence in platelet function in SHR.
Utilizing 30 mature SHRs (20-30 weeks of age) and 5 young SHRs (5-7 weeks) and same number of age matched NWRs, citrated blood samples were taken from carotid artery canulla for an analysis of platelet aggregability and 14C-serotonine (5-HT) release under pentobarbital anesthesia. ADP (1mg/kg) was injected into the jugular vein. After the injection, blood samples were taken at 3, 10 and 30min. for determination of platelet ADP and ATP contents.
Maximum intensity of ADP (100μM) induced platelet aggregation was significantly lower in SHR (46.5±11.0%, Mean±S. D.) than in NWR (59.3±5.6%) (p<0.05). 14C-5-HT release at 5min. after the addition of ADP (100μM) was significantly smaller in SHR (9.2±3.5%) than in NWR (21.5±5.1%) (p<0.05). Decrement in platelet ADP content after ADP injection was smaller in SHR (before: 2.1±0.3, at 30min.: 1.9±0.6μmoles/1011pl.) as compared with NWR (before: 2.1±0.7, at 30min.: 1.1±0.3) (p<0.05). In young SHR, ADP-induced platelet aggregability showed decreased tendency as compared with age matched NWR but this difference was not statistically significant. 14C-5-HT release was significantly decreased in young SHR than NWR.
These results suggest that the lower incidence in pulmonary microthromboembolism in SHR might be explained by in vitro platelet hypoaggregability and decreased platelet release reaction. Decreased platelet reactivity seen in young SHR seems to represent inherited defence mechanism against thrombus formation in SHR.
