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Platelet aggregation was produced in pial arterioles by exposing them to appropriately filtered light from a mercury lamp, following intravascular injection of sodium fluorescein. The dye acted as a target for the radiant energy and initiated a sequence of events resulting in the platelet aggregation. The aggregates adhered to the vessel in which they first appeared. When a microneedle punctured the brain adjacent to a subsequently irradiated arteriole, platelet aggregation was inhibited, even though the arteriole was not touched by the microneedle. Inhibition was manifested by prolongation of the exposure time required for the light-dye stimulus to initiate an adherent aggregate and by lengthening the time required for the aggregate to grow and totally block erythrocyte flow in the affected vessel. It is suggested that a material(s) diffuses from the zone of brain puncture, to and through the arteriolar wall, with a resultant inhibition of aggregation. It is noted that the inhibiting effect is reduced as the distance between puncture and wall increases.

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Effects of combined parenchymal and vascular injury on platelet aggregation in pial arterioles of living mice: evidence for release of aggregate-inhibiting materials.