BRIEF COMMUNICATIONINHIBITION OF COLLAGEN-INDUCED PLATELET AGGREGATION BY ARGATROBAN IN PATIENTS WITH ACUTE CEREBRAL INFARCTION
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MATERIALS AND METHODS
We studied 30 patients, mean age 73.3 ± 8.3 years (m ± SD, 16 males, 14 females) with acute cerebral infarction who were consecutively admitted to Hokudan Clinic and Awaji Hospital within 3 days after stroke. The diagnosis of cerebral infarction was confirmed by observation of typical neurological symptoms persisting for more than 24 hr. or longer with corresponding lesions depicted on computed tomographic scans or magnetic resonance images. The cerebral infarction was thought to be due to
RESULTS
In the in vitro study, the maximum of the collagen-induced aggregation curve increased in a thrombin-dose-dependent manner (Fig. 1). Sensitivity to collagen was enhanced in the presence of thrombin at sub-threshold concentrations. After addition of argatroban to normal PRP, the increased aggregation induced by thrombin was restored to the level without thrombin. In the presence of platelets preincubated with thrombin, the aggregation with collagen was inhibited by argatroban (Fig. 2).
DISCUSSION
Thrombin is one of the physiological agonists that may be present at the site of a vascular injury during the acute phase of cerebral infarction. The interaction of thrombin with platelets may be regarded both as an agonist-receptor reaction [6]. If a trace amount of thrombin is present in circulating blood, it does not induce platelet aggregation. The extent of the platelet response to thrombin appears to be a function of both the number of receptors cleaved and the time period over which they
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