| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥3,100,000 (Direct Cost: ¥3,100,000)
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| Research Abstract |
In order to clarify the mechanism of defect in a new type of platelet release mechanism abnormality reported by us in 1980-1981, intracellular Ca^<++>,[Ca^<++>]i, mobilization was analysed in cases of thrombin, A23187, stable thromboxane analog SAT_2 or arachidonate-induction using aequorin loading method. In presence of L mM Ca^<++>, patient (P) platelets showed normal [Ca^<++>]i elevation (influx and intracellular mobilization) in response to thrombin, but suppressed one to low concentration of A23187 or STA_2. The decreased mobilization in absence of Ca^<++> was enhanced to normal by addition of 2mM Ca^<++> or by adrenalin potentiation. TMB-8 which caused reduced aggregation similar to P platelets in normal platelets was not sensitive to adrenalin potentiation. Various but slight degree of abnormalities in [Ca^<++>]i mobilization were found in Bernard-Soulier syndrome, cyclooxygenase deficiency, and Hermansky-Pudlak syndrome, suggestkng different characters of Ca^<++> mobilization measured by present method. In conclusion P platelets were partially defective in Ca^<++> mobilization (probably Ca influx) in responses to A23187 or STA_2, and different from TMB-8 treated normal paltelets. Closer relation between[Ca^<++>]i mobilization and aggregation or release in various agonists is neccessary to be investigated.
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