PLATELET ACCUMULATION AND THROMBUS FORMATION AFTER MICROARTERIAL INJURY - AN EXPERIMENTAL-STUDY IN RABBITS

Patency rates and accumulation of P-32- labelled platelets were studie d in the central ear arteries of rabbits (which were not treated with antithrombotic agents) after three types of vascular injury: End to en d anastomosis, arteriotomy and superficial injury to the vessel wall t o expose the lamina elastica interna/juxtaluminal parts of the tunica media, arteriotomy and deep injury to the vessel wall to expose the de eper layers of the tunica media. The superficial and deep vessel injur ies were 5 mm long. Patency rates were 100% after end to end anastomos is and superficial injury, and 48% after deep injury. In a separate gr oup of vessels with deep injuries the time course of formation of occl usive thrombi was investigated: occlusion was already present 15 minut es after reperfusion in all but one of seven occluded vessels. Platele t 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 3 0 minutes, which was later followed by a gradual decrease. Platelet ac cumulation patterns indicating sustained thrombogenicity throughout th e measurement interval (embolization/reaccumulation patterns or late i ncreases in accumulation) were encountered in only three of 22 deeply injured vessels. We conclude that: to cause formation of occlusive thr ombus in otherwise healthy arteries and animals, a deep injury to the tunica media is necessary, and following reperfusion after repair of d amaged vessels the time course of the thrombotic challenge is short.