| Popis: |
When blood vessels are injured so that they bleed, circulating platelets adhere to the damaged vessel wall and aggregate within the first seconds. Ihe mechanism of the initial platelet aggregation remains uncertain. To investigate the initiation stage of haemostasis, the carotid arteries of rats were punctured with a 100 μm needle and free ATP, as an indicator of ADP, was measured in the emerging blood.This was brought into contact with luciferin-luciferase in a polyethylene tube, internal diameter 0.8 mm. The light produced at the blood/enzyme interface was measured with a sensitive photon - counting device which gave backgroundn counts of 1 photoelectron/sec. and could detect < 10-8M ATP in 2 μl bloodWhen an artery was injured, the emerging blood contained about 10-7 M ATP in a first peak after about 2 sec. After about one min. the ATP concentration rose to a second peak of about 5.10-6M This was decreased by heparin (500 U/kg body weight) or by chlorpromazine (1 mg/kg). The observations suggest that the second peak represents ATP released frem platelets. The source of ATP accounting for the first peak remains uncertain; possibly this ATP is released fran red cells undergoing high shear stress frem the haemodynamic effects of haemorrhage. |
