Effects of pulsed ultrasound on the frog heart: III. The radiation force mechanism.
Earlier studies have shown that a single, millisecond duration pulse of ultrasound delivered to the frog heart in vivo during systole can produce a reduction in the developed aortic pressure, while a pulse delivered during diastole can produce a premature ventricular contraction. The threshold for these effects is 5-10 MPa with a 5-ms pulse. Since cardiac tissues respond to mechanical stimulation, the objective of this study was to investigate acoustic radiation force as a possible mechanism for the observed effects of ultrasound on the frog heart. In two experiments, the radiation force exerted on the heart was varied by varying the ultrasonic frequency and the acoustic beam width. Results of these studies indicated that the rate of occurrence of the reduced aortic pressure effect was directly correlated with the magnitude of the radiation force exerted on the heart. A third experiment tested the radiation force mechanism directly by placing an acoustic reflector on the frog heart. The acoustic reflector maximized the radiation force delivered to the heart, but eliminated direct interaction of the ultrasound with the heart and experimentally eliminated heating and cavitation as mechanisms of action. The reduced aortic pressure effect was observed with the reflector on the heart, indicating that radiation force is capable of producing this effect. No premature ventricular contractions were observed with the acoustic reflector over the heart, suggesting that another property of the exposure may be responsible for this bioeffect.
Dalecki
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D
Department of Electrical Engineering, Rochester Center for Biomedical Ultrasound, University of Rochester, NY 14627, USA.
Raeman
C H
CH
Child
S Z
SZ
Carstensen
E L
EL
D000818:Animals; D001011:Aorta / Q000502:physiology; D004452:Echocardiography / Q000009:adverse effects; D006321:Heart / Q000502:physiology*; D011312:Pressure; D011894:Rana pipiens; D014465:Ultrasonics; D018879:Ventricular Premature Complexes / Q000209:etiology