ACCELERATION OF FIBRINOLYSIS BY ULTRASOUND IN A RABBIT EAR MODEL OF SMALL VESSEL INJURY

High frequency ultrasound has been previously shown to accelerate fibr inolysis in vitro at intensities that are potentially applicable for n oninvasive administration clinically. To extend these findings in vivo , we have investigated the effects of ultrasound on fibrinolysis induc ed by streptokinase in a rabbit model of small vessel injury. Full thi ckness puncture wounds were made in rabbit ears with a scalpel blade. The rabbits were rested for 2-3 hours after cessation of bleeding to a llow maturation of hemostatic plugs. Saline or streptokinase was then infused intravenously, and ultrasound was applied to some lesions at 1 MHz with a 50% duty cycle at 1 W/cm(2) net intensity. Ear lesions in rabbits treated with saline showed no bleeding after 30 minutes whethe r they were exposed to ultrasound or not. Streptokinase alone induced bleeding after 19.7 +/- 5.5 minutes. Application of ultrasound signifi cantly reduced the time to bleeding in streptokinase treated rabbits t o 7.5 +/- 3.9 minutes (p < .002). The times to bleeding with ''sham'' ultrasound (18.8 +/- 5.6 minutes) and heating of the ear (18.0 +/- 5.6 minutes) during streptokinase administration were not significantly d ifferent compared to streptokinase alone. Histologic examination revea led that application of ultrasound resulted in a mild increase in inte rstitial edema and accumulation of polymorphonuclear leukocytes but di d not cause vascular or other tissue damage. We conclude that the noni nvasive, percutaneous application of ultrasound significantly accelera ted streptokinase-induced fibrinolysis in this rabbit model of small v essel injury.