Platelet aggregation in cerebral arterioles after percussive brain trauma

Percussive injury to the cat brain is known to be accompanied by endothelial damage in pial arteries and arterioles distant from the percussed site. The damage is not accompanied by platelet aggregation, and it has been hypothesized that the injury may be associated with the production of antiaggregatory substances. In the present study, the pial vessels of percussed brains were exposed to radiant energy from a mercury lamp in the presence of intravascular sodium fluorescein. Both light and dye constitute a second source of microvascular injury which, by itself, has been shown to produce local platelet aggregation. The object of the present study was to see whether this aggregation was inhibited by the effects of prior brain percussion. Contrary to our expectation, we found that the initiation of aggregation was significantly enhanced by the prior injury, suggesting either a potentiation by one injury of the chemical effects of the other, or an enhancement by the first injury of the susceptibility of the vessels to physical damage by the second insult.