The Specificities of Aortic Intima Constituents Effecting ADP or Epinephrine-induced Platelet Aggregation

抄録

The specificities of extractable human uninvolved aortic intima constituents are summarized as follows in the effect on ADP or epinephrine-induced platelet aggregation.
I. Effects on ADP-induced aggregation
i) ADP-induced aggregation was inhibited by the extract.
ii) ADP aggregation inhibitory activity augmented progressively with increased incubation time of ADP and the extract at 25°C.
iii) The activity was stable at 37°C for at least 180 minutes. But it disappeared at 55°C for 10 minutes or at 100°C for 3 minutes.
iv) The activity was unstable below pH 5 or above pH 11.
v) Activity was detected when the extract and ADP were mixed before being added to PRP. II. Effects on epinephrine-induced aggregation
i) Epinephrine-induced aggregation was potentiated by the extract.
ii) The enhancement of the extract on epinephrine aggregation was not changed by incubation of the extract and epinephrine at 25°C.
iii) The enhancement disappeared at 100°C for 3 minutes.
iv) The effect was found not only in addition of the mixture of the extract and epinephrine to PRP, but also in sequential addition of the extract and epinephrine.
v) It was stable from pH 2 to pH 11.
vi) The constituent of the extract which potentiated epinephrine aggregation might be collagen with a lower concentration that could not cause platelet aggregation.
ADP aggregation inhibitory activity may limit the growth of intravascular thrombus. Epinephrine aggregation enhancement may induce the onset of atherosclerosis, myocardial infarction and cerebral thrombosis, whereas the enhancement may help the healing of endothelial damage by platelet aggregation forming thrombus.