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Platelet accumulation and thrombus formation after microarterial injury. An experimental study in rabbits.

Patency rats and accumulation of 32P-labelled platelets were studied in the central ear arteries of rabbits (which were not treated with antithrombotic agents) after three types of vascular injury: End to end anastomosis, arteriotomy and superficial injury to the vessel wall to expose the lamina elastica interna/juxtaluminal parts of the tunica media, arteriotomy and deep injury to the vessel wall to expose the deeper layers of the tunica media. The superficial and deep vessel injuries were 5 mm long. Patency rates were 100% after end to end anastomosis and superficial injury, and 48% after deep injury. In a separate group of vessels with deep injuries the time course of formation of occlusive thrombi was investigated: occlusion was already present 15 minutes after reperfusion in all but one of seven occluded vessels. Platelet accumulation ratios were significantly higher after deep injury than after end to end anastomosis or superficial injury. In deeply injured patent vessels, platelet accumulation reached a maximum after about 30 minutes, which was later followed by a gradual decrease. Platelet accumulation patterns indicating sustained thrombogenicity throughout the measurement interval (embolization/reaccumulation patterns or late increases in accumulation) were encountered in only three of 22 deeply injured vessels. We conclude that: to cause formation of occlusive thrombus in otherwise healthy arteries and animals, a deep injury to the tunica media is necessary, and following reperfusion after repair of damaged vessels the time course of the thrombotic challenge is short.