Thermal and metabolic responsiveness of Japanese quail embryos following periodic exposure to 2,450 MHz microwaves

Two studies were performed to determine if repeated exposure of the avian egg to microwaves can alter metabolism, temperature, and growth rate of embryos. Another aim was to supplement conventional heating with microwave heating and provide an optimal temperature for growth. Japanese quail (Coturnix coturnix japonica) eggs were exposed from day 1 through 15 of incubation (8 h/day) to sham or microwave (2,450 MHz) irradiation. Microwave exposures were at two power densities, 5 or 20 mW/cm2, and at three ambient temperatures (Tas), 30.0, 33.1, or 35.4 degrees C. Specific absorption rates for unincubated and 15-day-old incubated eggs were, respectively, 0.76 and 0.66 W kg-1 mW-1 cm-2 (i.e., 3.8 and 3.3 W/kg at 5 mW/cm2 and 15.2 and 13.2 W/kg at 20 mW/cm2). Eggs were concurrently sham exposed at each of five Tas, ranging from 27.9 to 37.5 degrees C. Tests were conducted during the 16th day of incubation (i.e., 1 day post-treatment), in the absence of microwaves, to determine metabolic rate of embryos and internal and external egg temperatures at different Tas. Repeated exposures to microwaves at 5 and 20 mW/cm2 at the same Ta (30 degrees C) increased wet-embryo mass on the 16th day by an average, respectively, of 9% and 61% when compared with predicted masses for embryos exposed at the same Ta in the absence of microwave radiation. There was no reliable indication, from post-treatment tests and comparisons with control embryos of similar mass, that repeated exposure to microwave radiation resulted in abnormal physiological development. Microwave radiation can be used to increase egg temperature and embryonic growth rate at Tas below normal incubation level without altering basic metabolic and thermal characteristics of the developing bird.     

EFFECTS OF MICROWAVES AND ELF MAGNETIC FIELD ON THE PHAGOCYTIC ACTIVITY OF VARIOUSLY TREATED RAT MACROPHAGES

The purpose of this study was to investigate the effects of 9450-MHz microwaves and extremely low frequency magnetic fields (ELFMF) on the phagocytic activity of rat macrophages in control rats and those treated with vitamins C and E. In the microwave group, 24 albino Wistar rats were exposed to microwaves (2.65 mW/cm², specific absorption rate [SAR]: 1.80 W/kg) for 1 h/day for 21 days. Thirty-two albino Wistar rats were divided into four groups (one control, three experimental) (n = 8). The rats in the first exposure group were only exposed to microwaves for 1 h per day for 21 days. In addition to exposure with microwaves as in the first experimental group, vitamins E and C (150 mg/kg/day) were injected intraperitoneally into the rats in the second and third exposure groups, respectively. In the magnetic field exposure group, 26 albino Wistar rats were divided into two groups: the sham (n = 12) and exposed groups (n = 14). The rats in the experimental group were exposed to ELFMF (50 Hz, 0.75 mT) for 3 h/day for 3 weeks. After completing the exposure period, the rats were sacrificed under ketalar anesthesia. The viability of isolated alveolar macrophages of rats in the microwave and ELF groups was determined and compared to sham groups. The results were analyzed with the Mann–Whitney U test. In the microwave group, the phagocytic activity in the experimental groups was found to be higher than the sham groups. However, with phagocytic activity in rats treated with both microwaves and vitamins, only the vitamin C group was significant (p < 0.05). In the magnetic field group, the phagocytic activity of rats exposed to ELFMF was lower than that of the sham group, but the results were not significant (p > 0.05). Rectal temperatures of microwaveexposed groups were found to be significantly higher compared to the control group (p < 0.05).     

Minimal changes in hypothalamic temperature accompany microwave-induced alteration of thermoregulatory behavior

This study probed the mechanisms underlying microwave-induced alterations of thermoregulatory behavior. Adult male squirrel monkeys (Saimiri sciureus), trained to regulate the temperature of their immediate environment (Ta) behaviorally, were chronically implanted with Teflon reentrant tubes in the medical preoptic/anterior hypothalamic area (PO/AH), the brainstem region considered to control normal thermoregulatory processes. A Vitek temperature probe inserted into the tube measured PO/AH temperature continuously while changes in thermoregulatory behavior were induced by either brief (10-min) or prolonged (2.5-h) unilateral exposures to planewave 2,450-MHz continuous wave (CW) microwaves (E polarization). Power densities explored ranged from 4 to 20 mW/cm2 (rate of energy absorption [SAR] = 0.05 [W/kg]/cm2]). Rectal temperature and four representative skin temperatures were also monitored, as was the Ta selected by the animal. When the power density was high enough to induce a monkey to select a cooler Ta (8 mW/cm2 and above), PO/AH temperature rose approximately 0.3 degrees C but seldom more. Lower power densities usually produced smaller increases in PO/AH temperature and no reliable change in thermoregulatory behavior. Rectal temperature remained constant while PO/AH temperature rose only 0.2-0.3 degrees C during 2.5-h exposures at 20 mW/cm2 because the Ta selected was 2-3 degrees C cooler than normally preferred. Sometimes PO/AH temperature increments greater than 0.3 degrees C were recorded, but they always accompanied inadequate thermoregulatory behavior. Thus, a PO/AH temperature rise of 0.2-0.3 degrees C, accompanying microwave exposure, appears to be necessary and sufficient to alter thermoregulatory behavior, which ensures in turn that no greater temperature excursions occur in this hypothalamic thermoregulatory center.     

Thermoregulatory consequences of long-term microwave exposure at controlled ambient temperatures

This study was designed to identify and measure changes in thermoregulatory responses, both behavioral and physiological, that may occur when squirrel monkeys are exposed to 2450-MHz continuous wave microwaves 40 hr/week for 15 weeks. Power densities of 1 or 5 mW/cm2 (specific absorption rate = 0.16 W/kg per mW/cm2) were presented at controlled environmental temperatures of 25, 30, or 35 degrees C. Standardized tests, conducted periodically, before, during, and after treatment, assessed changes in thermoregulatory responses. Dependent variables that were measured included body mass, certain blood properties, metabolic heat production, sweating, skin temperatures, deep body temperature, and behavioral responses by which the monkeys selected a preferred environmental temperature. Results showed no reliable alteration of metabolic rate, internal body temperature, blood indices, or thermoregulatory behavior by microwave exposure, although the ambient temperature prevailing during chronic exposure could exert an effect. An increase in sweating rate occurred in the 35 degrees C environment, but sweating was not reliably enhanced by microwave exposure. Skin temperature, reflecting vasomotor state, was reliably influenced by both ambient temperature and microwaves. The most robust consequence of microwave exposure was a reduction in body mass, which appeared to be a function of microwave power density.     

A small temperature rise may contribute towards the apparent induction by microwaves of heat-shock gene expression in the nematode Caenorhabditis Elegans

We have previously reported that low intensity microwave exposure (0.75-1.0 GHz CW at 0.5 W; SAR 4-40 mW/kg) can induce an apparently non-thermal heat-shock response in Caenorhabditis elegans worms carrying hsp16-1::reporter genes. Using matched copper TEM cells for both sham and exposed groups, we can detect only modest reporter induction in the latter exposed group (15-20% after 2.5 h at 26 degrees C, rising to approximately 50% after 20 h). Traceable calibration of our copper TEM cell by the National Physical Laboratory (NPL) reveals significant power loss within the cell (8.5% at 1.0 GHz), accompanied by slight heating of exposed samples (approximately 0.3 degrees C at 1.0 W). Thus, exposed samples are in fact slightly warmer (by < or =0.2 degrees C at 0.5 W) than sham controls. Following NPL recommendations, our TEM cell design was modified with the aim of reducing both power loss and consequent heating. In the modified silver-plated cell, power loss is only 1.5% at 1.0 GHz, and sample warming is reduced to approximately 0.15 degrees C at 1.0 W (i.e., < or =0.1 degrees C at 0.5 W). Under sham:sham conditions, there is no difference in reporter expression between the modified silver-plated TEM cell and an unmodified copper cell. However, worms exposed to microwaves (1.0 GHz and 0.5 W) in the silver-plated cell also show no detectable induction of reporter expression relative to sham controls in the copper cell. Thus, the 20% "microwave induction" observed using two copper cells may be caused by a small temperature difference between sham and exposed conditions. In worms incubated for 2.5 h at 26.0, 26.2, and 27.0 degrees C with no microwave field, there is a consistent and significant increase in reporter expression between 26.0 and 26.2 degrees C (by approximately 20% in each of the six independent runs), but paradoxically expression levels at 27.0 degrees C are similar to those seen at 26.0 degrees C. This surprising result is in line with other evidence pointing towards complex regulation of hsp16-1 gene expression across the sub-heat-shock range of 25-27.5 degrees C in C. elegans. We conclude that our original interpretation of a non-thermal effect of microwaves cannot be sustained; at least part of the explanation appears to be thermal.     

Core temperature is regulated, although at a lower temperature, in rats exposed to hypergravic fields

1. In rats acclimated to 23 degrees C (RT rats) or 5 degrees C (CA rats), core temperature (Tc), tail temperature (Tt) and oxygen consumption (VO2) were measured during exposure to a hypergravic field. 2. Rats were exposed for 5.5 h to a 3 g field while ambient temperature (Ta) was varied. For the first 2 h, Ta was 25 degrees C; then Ta was raised to 34 degrees C for 1.5 h. During this period of warm exposure, Tc increased 4 degrees C in both RT and CA rats. Finally, Ta was returned to 25 degrees C for 2 h, and Tc decreased toward the levels measured prior to warm exposure. 3. In a second experiment at 3 g, RT and CA rats were exposed to cold (12 degrees C) after two hours at 25 degrees C. During the one hour cold exposure, Tc fell 1.5 degrees C in RT and 0.5 degree C in CA rats. After cold exposure, when ambient temperature was again 25 degrees C, Tc of RT and CA rats returned toward the levels measured prior to the thermal disturbance. 4. Rats appear to regulate their temperature, albeit at a lower level, in a 3 g field.     

Nocturnal shifts in thermal and metabolic responses of the immature rat

Immature rats were tested at 2, 7, 11, and 15 days of age to determine steady-state thermoregulatory responses during light (L) and dark (D) phases of the daily cycle. Pups were housed with dams in a vivarium illuminated from 0700 to 1900 h. During each phase tests began approximately 1 h after the change in the light conditions of the vivarium. Duration of each test was approximately 7 h. Rats were tested individually in temperature-controlled cylinders at ambient temperatures (Ta) = 25.0, 30.0, 32.5, and 35.0 degrees C. Both colonic (Tco) and tail skin temperatures of each animal were measured continuously. O2 content of effluent air from each cylinder was determined to provide an estimate of metabolic rate (M). Immature rats, at 2 to 11 days of age, exhibited significant L:D differences in M and Tco. However, no significant L:D differences in these responses were noted at 15 days of age. In every case, nocturnal increases in Tco were associated with a rise in M. L:D differences in Tco response were not attributed to a significant change in total thermal conductance. These data support the conclusion that the immature rat exhibits daily variation in metabolic rate, which is the primary contributor to L:D shifts in Tco.     

Thermoregulatory adjustments in squirrel monkeys exposed to microwaves at high power densities

The present study was undertaken to investigate the thermal adjustments of squirrel monkeys exposed in a cold environment to relatively high energy levels of microwave fields. The animals (Saimiri sciureus) were equilibrated for 90 min to a cool environment (Ta = 20 degrees C) to elevate metabolic heat production (M). They were then exposed for brief (10-min) or long (30-min) periods to 2,450-MHz continuous-wave microwaves. Power densities (MPD) were 10, 14, 19, and 25 mW/cm2 during brief exposures and 30, 35, 40, and 45 mW/cm2 during long exposures (rate of energy absorption: SAR = 0.15 [W/kg]/[mW/cm2]). Individual exposures were separated by enough time to allow physiological variables to return to baseline levels. The results confirm that each microwave exposure induced a rapid decrease in M. In a 20 degree C environment, the power density of a 10-min exposure required to lower M to approximate the resting level was 35 mW/cm2 (SAR = 5.3 W/kg). During the long exposures, 20 min was needed to decrease M to its lowest level. Cessation of irradiation was associated with persistence of low levels of M for periods that depended on the power density of the preceding microwave exposure. Vasodilation, as indexed by changes in local skin temperature, occurred at a high rate of energy absorption (SAR = 4.5 W/kg) and was sufficient to prevent a dramatic increase in storage of thermal energy by the body; vasoconstriction was reinstated after termination of irradiation. Patterns of thermophysiological responses confirm the influence both of peripheral and of internal inputs to thermoregulation in squirrel monkeys exposed to microwaves in a cool environment.     

Effects of hypoxia and cold acclimation on thermoregulation in the rat.

The effects of hypoxia (inspired O2 fraction = 0.12) on thermoregulation and on the different sources of thermogenesis were studied in rats before and after periods of 1-4 wk of cold acclimation. Measurements of metabolic rate (VO2) and body temperature (Tb) were made at 5-min intervals, and shivering activity was recorded continuously in groups of rats subjected to three protocols. In protocol 1, rats were exposed to normoxia to an ambient temperature (Ta) of 5 degrees C for 2 h. In protocol 2, at Ta of 5 degrees C, rats were exposed for 30 min to normoxia, then for 45 min to hypoxia, and finally for 30 min to normoxia. In protocol 3, in the non-cold-acclimated (NCA) rats, Ta was decreased from 30 to 5 degrees C in steps of 5 degrees C and of 30-min duration while in cold-acclimated (CA) rats at 5 degrees C for 4-wk, Ta was increased from 5 to 30 degrees C in steps of 5 degrees C and of 30-min duration. Recordings were made in normoxia and in hypoxia on different days in the same animals. The results showed that 1) in NCA rats, cold exposure in normoxia induced increases in VO2 and shivering that were proportional to the decrease in Ta; 2) in CA rats in normoxia, for a given Ta, VO2 and Tb were higher than in NCA rats, whereas shivering was generally lower; and 3) in both NCA and CA rats, hypoxia induced a transient decrease in shivering and a sustained decrease in nonshivering thermogenesis associated with a marked decrease in Tb that was about the same in NCA and CA rats. We speculate that hypoxia acts on Tb control to produce a general inhibition of thermogenesis. Nonshivering thermogenesis is markedly sensitive to hypoxia, especially demonstrable in CA rats; a recovery or even an increase in shivering can compensate for the decrease in nonshivering thermogenesis.     

Microwave-induced increase of water and conductivity in submaxillary salivary gland of rats

Hypersalivation is an important mechanism for heat dissipation by animals without sweat glands. The water content and conductivity (at 20 kHz) in sub-maxillary salivary gland (SSG) and in other tissues were investigated in adult male rats exposed to microwaves (2880 MHz, 1.5 μs pulses at 1000 Hz) or to conventional heat at 40 °C. Eighty rats in one series were exposed, one at a time, for 30 min to microwaves producing a specific absorption rate (SAR) of 4.2,6.3,6.8,8.4,10.8 or 12.6 W/kg. Fifty rats were sham-exposed under similar environmental conditions. In the second series, ten rats were sham-exposed, 33 rats were exposed, one at time, for 15, 30 or 60 min to microwaves at a SAR of 9.5 W/kg, and 32 rats were exposed for similar periods to conventional heat at 40 °C. In rats of the first series colonic temperatures were elevated significantly at a SAR of 4.2 W/kg, while SSG water content and conductivity increased significantly at SAR values of 6.3 W/kg and higher. In the second series of experiments increases in colonic temperature and SSG water content were greater after 15 and 30 min of microwave exposure than after exposure to heat. Also, SSG conductivity was significantly depressed by heat and significantly increased by microwaves after exposure for 15 or 30 min. The results support the hypothesis that water content and conductivity of SSG of rats can be used as a sensitive specific test of a microwave induced thermal response.     

The effects of acclimation temperature on pituitary and plasma beta-endorphin in rats at 32.5 degrees C

Endocrine and thermoregulatory responses were studied in male rats exposed to heat (32.5 +/- 0.1 degrees C) from acclimation temperatures of either 24.5 +/- 0.1 degrees C or 29.2 +/- 0.1 degrees C. After 1 hr in the heat, evaporative water loss and tail skin temperature changes in the 24.5 degrees C acclimated rats were greater than in the 29.2 degrees C acclimated rats; both groups displayed similar changes in metabolic rate and rectal temperature. At the respective acclimation temperatures, 29.2 degrees C rats displayed lowered plasma thyroid hormones, elevated beta-endorphin-like immunoreactivity (beta-END-LI) in the plasma, neurointermediate and anterior lobes of the pituitary gland, and no change in plasma corticosterone levels compared to 24.5 degrees C rats. After exposure to 32.5 degrees C for 1 hr, both groups of rats maintained similar plasma corticosterone levels; however, only the 24.5 degrees C group increased plasma thyroxine and beta-END-LI. These data suggest that beta-endorphin may be involved in body temperature regulation during acclimation to elevated environmental temperatures.     

Increased serum enzyme activity in microwave-exposed rats

Heat stable serum enzymes were studied in rats exposed to microwaves (2.45 GHz, 120 Hz amplitude modulated) 24 hr after a single 4-hr exposure or immediately after 3 and 10 exposures to 0.1 to 55 mW/cm2. In addition, stable colonic temperature at 41.5 degrees C for 30 min was maintained by microwave exposure in a group of five rats under barbiturate anesthesia. Alkaline phosphatase and lactic dehydrogenase did not increase as a result of microwave exposure. Increased serum glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT) were noted in the 41.5 degrees C group 24 hr after exposure. A threshold body temperature for acute cellular injury after microwave exposure was demonstrated. The acute cellular injury could be in the liver. These mild elevations in the serum enzyme levels (mean +/- SE, GOT = 167 +/- 40 U/liter: GPT = 74 +/- 26 U/liter) indicated that the injuries were not accompanied by any significant sequelae in the rat. From this threshold and colonic temperature (41.5 degrees C for 30 min) in barbiturate-anesthetized, microwave-exposed rats, we derived a tentative threshold for the whole-body average absorption rate at 14 W/kg (70 mW/cm2 at 2.45 GHz for adult rats) for 4 hr. This tentative threshold is subject to changes by duration of exposure and by compounding variables influencing maintenance of body temperature.     

Quantitative changes in potassium,sodium, and calcium in the submaxillary salivary gland and blood serum of rats exposed to 2880-MHz microwave radiation

Na⁺, K⁺, and Ca²⁺ concentrations in the blood serum and submaxillary salivary gland (SSG) were investigated in adult, male rats exposed to 2880-MHz microwaves modulated with 1.5-μs pulses at a pulse repetition rate of 1000 Hz or in a hyperthermal environment. Rats were exposed, one at a time, for 30 min to microwaves producing a specific absorption rate (SAR) of: 4.2, 6.3,6.8,8.4, 10.8, or 12.6 W/kg, or were sham exposed under similar environmental conditions. In a second series, one group of rats was exposed singly for 15, 30, or 60 min to microwaves producing an SAR of 9.5 W/kg and other rats were exposed for similar periods at 40 °C; and 10 rats were sham exposed. Flame photometric analysis indicated that the thresholds of microwave radiation required to induce a change in Na⁺, K⁺, and Ca²⁺ concentrations in the salivary glands are 6.8, 6.8, and 6.3 W/kg, respectively. The directions of Na⁺, K⁺, and Ca²⁺ ion shifts in exposed rats' salivary glands are similar, whether affected by microwaves or hyperthermia. Greater changes in Na⁺ and K⁺ concentrations in SSG of rats exposed to microwaves for 15 and 30 min were found than in those exposed at 40 °C. On the other hand, exposure to hyperthermia at 40 °C or to microwaves for 1 h caused Na⁺ concentration to be increased by 68.7 and 59.5% and K⁺ concentration to be decreased by 29.6 and 21.7%, respectively.     

Effects of cold and capsaicin desensitization on prostaglandin E hypothermia in rats

Intraperitoneal injection of prostaglandin E1 (PGE) produces a transient hypothermia in rats that lasts 1-2 h. Rats exposed to an ambient temperature (Ta) of 26 degrees C displayed a decrease in rectal temperature (Tre) of 0.95 +/- 0.12 degrees C (SE) after injection with PGE (100 micrograms/kg ip). Hypothermia was produced mainly by heat losses, as indicated by increases in tail blood flow. At Ta of 4 degrees C, PGE produced a comparable fall in Tre of 1.00 +/- 0.14 degrees C. However, in the cold the hypothermia was caused solely by decreases in heat production. These results indicate that the PGE-induced hypothermia is not the result of a peripheral vasodilation induced by the direct action of PGE on the tail vascular smooth muscle but is a central nervous system-mediated response of the thermoregulatory system induced by PGE within the peritoneal cavity. Capsaicin injected subcutaneously induces a transient hypothermia in rats because of stimulation of the warm receptors. If administered peripherally in sufficient amounts, it is reputed to impair peripheral warm receptors so that they become desensitized to the hypothermic effects of capsaicin. We measured PGE-induced hypothermias in rats both before and after capsaicin desensitization at Ta of 26 degrees C. Before desensitization the hypothermia was -1.14 +/- 0.12 degrees C, whereas after capsaicin treatment the PGE-induced hypothermia was -0.34 +/- 0.17 degrees C. The biological effects of capsaicin are diverse; however, based on current thinking about the thermoregulatory effects of capsaicin desensitization, our results indicate that peripheral warm receptor pathways are in some manner implicated in the hypothermia induced by intraperitoneal PGE.     

Effects of short-term cold exposure on pineal biosynthetic function in rats

In light of recent studies demonstrating stress-induced changes in pineal indoleamine metabolism, we tested the effect of acute cold stress on pineal biosynthetic function. Adult male rats were subjected to 30, 60, or 120 min of cold exposure (Ta = 2 degrees C) during either the light or dark phase of the daily photoperiodic cycle. Controls were kept at room temperature (22 +/- 2 degrees C). Animals were killed by decapitation and pineals were analyzed by radioimmunoassay for melatonin content and by radioenzymeassay for the activity of N-acetyltransferase (NAT). Cold exposure during the day elicited no significant changes in pineal indoleamine metabolism. Exposure to cold for 1 hr during the second hour after lights off slightly increased pineal melatonin content, without a concomitant change in NAT activity. Rats exposed to 2 hr of cold beginning 2 hr after lights off, however, displayed a 50% reduction in NAT activity, whereas pineal melatonin content remained unchanged. The paradoxical response of pineal NAT activity and melatonin content are not uncommon when rats are exposed to adverse stimuli.     

Increased thermoregulatory responsiveness in cold adapted but not in hyperthyroid hypermetabolic rats

Cold-adapted (CA) rats, unlike non-adapted (NA) ones, give exaggerated metabolic response to acute cold exposure, with paradoxical "overshoot" core temperature (Tc) rise in the cold, and they also give enhanced hyperthermia to central injection of prostaglandin E1 (PGE1). The adaptation-dependent differences might be explained either by the high thermogenic capacity of peripheral tissues in CA rats or by differences in the central processing of regulatory signals. If high tissue metabolism sufficiently explains the extreme responses of CA animals, other hypermetabolic states (with high resting metabolic rate, RMR), e.g. hyperthyroidism, should also be accompanied by enhanced reactions. In the present study thermoregulatory responses to acute cold exposure or to PGE1 were compared in hypermetabolic CA, similarly hypermetabolic thyroxine-treated (T4) and control non-hypermetabolic NA rats (mean RMR = 8.12, 8.47 and 6.03 W kg(-1), respectively). Cold exposure was followed by paradoxical core temperature (Tc) rise of 0.5 to 0.7 degrees C only in CA rats, but by Tc fall (0.8 to 2.1 degrees C) in NA and T4 animals. Identical central stimuli (PGE1) induced larger elevations of Tc and metabolic rate in CA rats than in similarly hypermetabolic T4 or in non-hypermetabolic NA animals (mean Tc rise of 1.9 degrees C in CA vs. 0.9 degrees C in T4 and 1.0 degrees C in NA rats). Vasodilatation thresholds were also similar in NA and T4, but lowered in CA animals. A hypermetabolic status, per se, does not seem to explain the enhanced thermoregulatory responsiveness of CA animals, adaptation-induced central regulatory changes may be more important for the "overshoot" phenomenon.     

Ventilatory and metabolic responses to cold and hypoxia in intact and carotid body-denervated rats.

The effects of hypoxia on thermoregulation and ventilatory control were studied in conscious rats before and after carotid denervation (CD). Measurements of metabolic rate (VO2), ventilation (V), shivering intensity (SI), and colonic temperature (Tc) were made in groups of eight rats subjected to three protocols. In protocols 1 and 2, at ambient temperature (Ta) of 25 and 5 degrees C, respectively, rats were exposed to normoxia and hypoxia [inspired O2 fraction (FIO2) 0.13-0.11]. In protocol 3, Ta was decreased from 25 to 5 degrees C in 30-min steps of 5 degrees C. Recordings were made in normoxia and hypoxia (FIO2 0.12). The results show that in both intact and CD rats 1) in normoxia, cold exposure increased VO2, V, and SI, and these increases were proportional to the decrease in Ta; 2) hypoxia induced only a transient decrease in SI, and, for a given Ta, VO2 was reduced whereas V and SI were increased; and 3) in CD rats, V increased less during cold exposure in both normoxia and hypoxia; VO2 and Tc were more depressed during hypoxia. It is concluded that 1) the interaction between Ta and FIO2 in the control of V is partly dependent on the carotid body afferents, 2) shivering thermogenesis may be transiently affected by hypoxia independently of the carotid body afferents, and 3) nonshivering thermogenesis may be directly inhibited by hypoxia, especially during cold exposure.     

Acute effects of pulsed microwaves and 3-nitropropionic acid on neuronal ultrastructure in the rat caudate-putamen

Ultrastructure of the medium sized "spiny" neuron in rat dorsal-lateral caudate-putamen was assessed after administration of 3-nitropropionic acid (3-NP) and exposure to pulsed microwaves. Sprague-Dawley male rats were given two daily intraperitoneal doses of 0 or 10 mg/kg 3-NP and 1.5 h after each dose were exposed to microwave radiation at a whole body averaged specific absorption rate (SAR) of 0 (sham exposure), 0.6, or 6 W/kg for 30 min. Microwave exposure consisted of 1.25 GHz radiation delivered as 5.9 micros pulses with repetition frequency 10 Hz. Tissue samples taken 2-3 h after the second sham or microwave exposure showed no injury with light microscope methods. Blinded qualitative assessment of ultrastructure of randomly selected neurons from the same samples did reveal differences. Subsequent detailed, quantitative measurements showed that, when followed by sham exposure, administration of 3-NP significantly increased endoplasmic reticulum (ER) intracisternal width, ER area density, and nuclear envelope thickness. Microwave exposure at 6 W/kg alone also significantly increased these measures. Exposure of 3-NP treated animals at 6 W/kg significantly increased effects of 3-NP on ultrastructure. Although exposure at 0.6 W/kg alone did not affect ultrastructure measures, exposure of 3-NP treated animals at 0.6 W/kg reduced the effects of 3-NP. We concluded that 3-NP changed neuronal ultrastructure and that the microwave exposures used here changed neuronal ultrastructure in ways that depended on microwave SAR and neuron metabolic status. The apparent cancellation of 3-NP induced changes by exposure to pulsed microwaves at 0.6 W/kg indicated the possibility that such exposure can protect against the effects of mitochondrial toxins on the nervous system.     

The relationship of decreased serum thyrotropin and increased colonic temperature in rats exposed to microwaves

Although decreased serum thyrotropin (TSH) concentration has been found to be part of the endocrine response pattern in rats exposed to microwaves and other stimuli, the response of individual endocrine organs was not activated simultaneously by a given irradiance. Therefore, analytical evaluation of the function of endocrine organs individually as well as collectively is required to characterize the extent of biological involvement in microwave exposure. We have studied the changes in TSH concentration in unanesthetized rats exposed to 2.45 GHz amplitude modulated (120 Hz) microwaves in the far field for 2 and 4 h, between 0 and 55 mW/cm2, and from 1 to 10 times to demonstrate any possible cumulation, acclimation, or sensitization process. Ether inhalation was administered to test the responsiveness of TSH in groups of rats that failed to respond to microwave exposure by lowering TSH concentration. In addition, groups of rats were sampled 24 h after microwave exposure to test the persistency of the microwave effect on serum TSH concentration. Results showed that TSH concentration decreased in rats after microwave exposure. Influence of microwave exposure on serum TSH concentration was independent of the number of exposures indicating absence of cumulation, acclimation, or sensitization. The microwave effect on serum TSH could be dependent on duration of exposure. Decreased TSH concentration was usually accompanied by increased colonic temperature. For 4-h exposure, the lowest irradiance was 20 mW/cm2 or a 0.3 degree C increase in colonic temperature independent of the number of exposures. For 2-h exposure, the lowest irradiance was 30 mW/cm2 or a 1.1 degree C increase in colonic temperature regardless of the number of exposures. All the rats exposed at 10 mW/cm2 for 2 h had a lower TSH concentration than those of sham-exposed rats. Occasionally, significant reduction in TSH concentration could not be found in rats exposed to 20 or 25 mW/cm2 for 2 h. None of the rats exposed at an irradiance lower than 10 mW/cm2 had any change in TSH concentration. Failure of change in TSH concentration in response to microwave exposure was not a reflection of a deficiency since these rats responded to ether inhalation by lowering their TSH concentration. The effect of microwave exposure on TSH concentration was not persistent after exposure. The relation between TSH concentration and colonic temperature was curvilinear (exponential). From these results, two mechanisms and their implications for man were discussed.(ABSTRACT TRUNCATED AT 400 WORDS)     

Thermoregulation in the cold after physical training at different ambient air temperatures

Since human thermoregulation at rest is altered by cold exposure, it was hypothesized that physical training under cold conditions would alter thermoregulation. Three groups (n = 8) of male subjects (mean age 24.3 +/- 0.9 years) were evaluated: group T (interval training at 21 degrees C), group CT (interval training at 1 degrees C), and group C (no training, equivalent exposure to 1 degrees C). Each group was submitted, before and after 4 weeks of interval training (5 d/week), to a cold air test at rest (SCAT) (dry bulb temperature (Tdb) = 1 degrees C) for a 2-h period for evaluation of the thermoregulatory responses. During SCAT, after the training/acclimation period, group T exhibited a higher rectal temperature (Tre) (P < 0.05) without significant change in mean skin temperature (Tsk) whereas metabolic heat production (M) was higher at the beginning of the SCAT (P < 0.05). For group CT, no thermoregulatory change was observed. Group C showed a lower Tre (P < 0.05) without significant change in either Tsk or in M, suggesting the development of a hypothermic general cold adaptation. This study showed, first, that the cold thermoregulatory responses induced by an interval training differed following the climatic conditions of the training and, second, that this training performed in the cold prevented the development of a general cold adaptation.