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Ultrastructure and behaviour of platelet thrombi in injured arteries.

Abstract 
An electron microscopy study was made of cerebral arteries in the rabbit after injuries adequate to produce platelet thrombi. 
 
Minor mechanical injuries, that is to say injuries which produced thrombi briefly without extravasation of blood, all showed a breach in the artery wall through which a haemostatic plug projected internally and externally; damage to endothelium and media adjacent to breach was invariable. 
 
Electrical injuries were inflicted by applying a unipolar electrode 0·0457 mm. in diameter to the pial surface of a cortical artery. With cathodal stimuli, ranging from 3-10 V d.c. 1-50 μA the arteries contracted and white bodies formed; they persisted for a few minutes up to 180 min. Because of the variable duration inhibitors were difficult to evaluate. When thrombi had ceased to form adenosine diphosphate (ADP), often in minute concentrations, would provoke the return of thrombus formation. 5-Hydroxytryptamine had a less constant effect. Electron microscopic examination showed a loss of endothelium and extensive damage to muscle cells of media at the site of injury. The media often contained platelets and sometimes red cells. Platelet thrombi were present on the wall denuded of endothelium and adjacent to it. In specimens obtained a few minutes after injury platelets showed remarkable ballooning by electron translucent contents. In lesions which had ceased to form thrombi spontaneously, but which were in a state when reactivation with ADP was expected, a rim of platelets covered the site of injury. 
 
Anodal stimuli had usually to be stronger to produce comparable thrombus formation. Vasoconstriction was never seen. Endothelium showed enormous distension with loss of the luminal membrane and apparent explosion of contents inwards. In very early lesions a rim of amorphous material was found on the internal elastic lamina and stuck in tufts to the most closely adjacent platelets, though less so to those more distant. Medial injury was always found. Ballooning of platelets in the earliest injuries was not observed. In other respects the changes were similar to those found with cathodal injury.