Intravenous bolus injection of 2.5% fluorescein sodium, 2ml/kg, constantly produced platelet thrombi at the site of microvasculature where the filtered light, 20.7mW/mm2 in intensity, had been radiated. The phenomena were observed with an intravital microscopy and recorded on VTR which allowed better analysis in playback mode. Using this model developed by Sato and Ohshima, the inhibitory effect of Trapidil on thrombus formation in the venules, 40-60μm in diameter, was studied in the rat mesentery. Trapidil was administered either intravenously (group A) or orally (group B). Two mg/kg/min of intravenous infusion of Trapidil induced significant decrease in blood pressure. The initiation time of thrombus formation, ti, was significantly prolonged compared with that of control. Marked retardation of the time to stop flow was also observed. In the case of intravenous infusion of Trapidil, 0.2mg/kg/min, blood pressure remained unchanged. Although no difference in ti was found between Trapidil loaded and control rats, is was significantly prolonged in Trapidil group. In group B, 30mg/kg/day of Trapidil were given orally for 6 days. Although no difference in ti was observed between Trapidil loaded and control rats, is was significantly prolonged in Trapidil group. The results indicated that Trapidil inhibited both initiation and growth of thrombus formation in this model. In group A, no significant difference in is was found between high and low dose of Trapidil. Decrease in flow velocity secondary to significant drop in blood pressure might be responsible for this difference.
