Previous studies have shown that 40 kHz ultrasound at low intensity enhances enzymatic fibrinolysis in vitro and in vivo and causes reversible vasodilation. We have now investigated the role of the nitric oxide system in vasodilation stimulated by ultrasound. After ligation of the femoral artery of rabbits, tissue perfusion in the gracilus muscle as measured with a laser Doppler probe decreased from 13.7 ±0.4U to 4.5 ±1.4U by 120 minutes, but application of 40 kHz ultrasound then improved perfusion to 12.1 ±0.5U after 60 minutes of application. Similarly, tissue pH decreased from a normal value of 7.41 ± 0.2 to 7.0 ±0.3U by 120 minutes and ultrasound improved pH to 7.34 ±0.3U after 60 minutes. Histologie sections showed vasodilation of capillaries in ultrasound exposed muscle. As quantitated by morphometric analysis, the mean circumference of individual capillaries increased from 18.9 ±2.3 mm at baseline to 23.1 ±3.7 mm after ultrasound (p < .01). The ultrasound-induced effects on tissue perfusion, pH, and capillary circumference were completely prevented by pre-treatment of the rabbits by L-NAME, a nitric oxide synthase inhibitor. Direct assay of nitric oxide synthase activity in muscle measured by conversion of ?H-arginine to citrulline showed a 2.2 fold increase after ultrasound exposure (p < .01 ). There was, however, no effect after pretreatment with L-NAME. We conclude the application of 40 kHz ultrasound to ischémie muscle induces nitric oxide synthase resulting in capillary dilation, improved tissue perfusion, and reversal of acidosis. The ability of ultrasound to enhance thrombolysis and improve tissue perfusion by causing vasodilation suggests that it may a useful adjunct to thrombolytic therapy.
|Original language||English (US)|
|Issue number||11 PART II|
|State||Published - Dec 1 2000|
ASJC Scopus subject areas
- Cell Biology