int. j. radiat. biol 2000, vol. 76, no. 4, 575 ± 579
Pain relief caused by millimeter waves in mice: results of cold
water tail ick tests
M. A. ROJAVIN, A. A. RADZIEVSKY*, A. COWAN† and M. C. ZISKIN
(Received 7 April 1999; accepted 4 June 1999)
Abstract. study, naloxone exhibited its inhibitory activity in
Purpose : To nd out if millimeter waves can decrease experimental
a dose-dependent manner and stereoselectively
pain response in mice using cold water tail ick test.
( Õ )-naloxone exerted the eÚect, while the biologic-
Materials and methods : Male Swiss albino mice (15 mice per group)
ally inactive enantiomer ( +)-naloxone did not.
were exposed to continuous millimeter waves at a frequency of
Any new method of pain relief is clinically import-
61.22 GHz with incident power densities (IPD) ranging from
0.15 to 5.0 mW/cm
2
for 15min or sham exposed. Latency of ant, especially a non-pharmacological non-invasive
tail withdrawal in a cold water (1
Ô
0.5ßC) tail ick test was
procedure such as mm waves. To verify some of the
measured before the exposure (baseline) and then four times
clinical reports, published mostly in the Russian
after the exposure with 15min breaks.
language (Lyan and Votoropin 1996, Shliapak et al.
Results : The mean latency of the tail ick response in mice
1996, Vinogradov et al. 1993), Lyan and Votoropin
exposed to millimeter waves was more than twice that of sham-
exposed controls ( p < 0.05). This eÚect was proportional to the 1996, Shliapak et al. 1996, Bakalyuk 1997), a double-
power of millimeter waves and completely disappeared at an
blind phase I pilot clinical trial was conducted with
IPD level of < 0.5 mW/cm
2
. Pretreatment of mice with the
healthy human volunteers, and it was found that mm
opioid antagonist naloxone (1mg/kg i.p.) blocked the eÚect of
waves suppressed experimental pain (cold pressor
millimeter waves.
test) in human subjects (Radzievsky et al. 1999).
Conclusions : Results suggest that the antinociceptive eÚect of
millimeter waves is mediated through endogenous opioids. Based on the above ndings, the present authors
have formulated the hypothesis that mm waves trig-
ger the release of endogenous opioids, and this results
1. Introduction
in decreased pain sensitivity in humans and animals.
In the present work, the mouse cold water tail ick Electromagnetic millimeter waves (mm waves) with
low ( < 20mW) output power have been used for assay was chosen to test this hypothesis.
medical purposes for the last 15 years, with sedation
and pain relief being the most frequent therapeutic
2. Materials and methods
eÚects registered in the majority of patients
2.1. Animals
(Pakhomov et al. 1998, Rojavin and Ziskin 1998).
Pain relief is usually reported by patients with various
Male Swiss albino mice (22–25 g; Ace
diseases after the rst two to three sessions of mm
Laboratories, Doylestown, PA) were used. The
wave exposure, which suggests that a certain non-
animals were acclimated for 3–4 days to a 12/12h
specic mechanism of pain relief is triggered by this
light/dark cycle at an ambient temperature of
method of treatment.
21 Ô 1ß C with an appropriate diet and drinking water
No laboratory experiments aimed at studying the
ad libitum. The Institutional Animal Care and Use
above eÚects are known of, but several related obser-
Committee approved the protocol of this experiment.
vations have been made in animals: mm waves
increase the duration of ketamine or chloral hydrate
2.2. Reagents
anaesthesia (Rojavin and Ziskin 1997) and decrease
experimental itch (Rojavin et al. 1998). In both cases,
Naloxone hydrochloride was obtained from Astra
the eÚects of mm waves were blocked by the opioid
Pharmaceutical (Westborough, MA, USA).
antagonist naloxone indicating that endogenous
opioids were probably involved. In the latter
2.3. Experimental set-up
*Author for correspondence.
The characteristics of the exposure chamber and
e-mail: aradziev@unix.temple.edu
experimental set-up have been previously described
Richard J. Fox Center for Biomedical Physics and
(Rojavin and Ziskin 1997). Briey, the exposure,
†Department of Pharmacology, Temple University School of
Medicine, 3400 N. Broad Street, Philadelphia, PA 19140, USA. sham exposure and testing of mice were conducted
International Journal of Radiation Biology ISSN 0955-3002 print/ISSN 1362-3095 online © 2000 Taylor & Francis Ltd
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