Effect of Pulsed Low-Power Ultrasound on Growing Tissues

Abstract

Pulsed ultrasound at 2.25 MHz was delivered by a transducer having an average power output of 1.5 mW to developing rat embryos in utero for 5 min and to larval and pupal stages of Drosophila melanogaster for 2.5 min. These exposures in some instances were lethal, in others growth inhibiting, and in still others, produced no detectable effect. Effects were dependent on stage of development at insonation.

Auditory Evoked Potential Alterations Induced by Pulsed Ultrasound

“…Earlier work in our laboratories using the same methodology and equipment to be described below, demonstrated a statistically significant (P < .05) hearing deficit in ten animals sonicated in utero as compared with ten unsonicated controls at all auditory frequency levels tested (2,4,8,12,16, and 20 kHz). Because this work indi¬ cated a possible effect of ultrasound on the fetus, the study was repeated using more animals, with the addition of even more stringent guidelines, bet¬ ter mensuration of the applied ultra¬ sound, and light and electron micro¬ scopic evaluation of the cochlear organ of Corti.…”

Sister Chromatid Exchanges in Human Lymphocytes After Exposure to Diagnostic Ultrasound

“…Investigators have been unable to demonstrate deleterious effects of ultrasound on human chromosomes (2)(3)(4)(5)(6)(7). However, as recently reported (8,9), exposure to pulsed ultrasound generated by a commercial diagnostic instrument appeared to have deleterious effects on rapidly growing mammalian and insect tissues. We have detected disturbances in HeLa cell DNA and in the growth characteristics of C3H mouse cell cultures exposed to ultrasound in the diagnostic range (10).…”

“…The proposal that this direct CNS effect results from the action of TRH as a neurotransmitter or neuromodulator has been supported by several observations: (i) TRH is present in the brain of several vertebrate and nonvertebrate species, including those that lack a thyroid gland (2); (ii) TRH is localized within neurons (3); (iii) TRH is concentrated within, and can be released from, preparations of synaptosomes (4, 5); (iv) high-affinity stereoselective TRH binding sites are present within the brain (6); and (v) exogenous applications of TRH can alter central neuronal excitability (7,8). In previous studies (8), we indicated that microiontophoretic application of TRH is associated with a decrease in spontaneous or glutamate-evoked activity in several brain regions-an observation that has prompted further examination of the specificity of the action of TRH.…”