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Sustained whole-body exposure of anesthetized rats to 35-GHz radiofrequency radiation produces localized hyperthermia and hypotension, leading to circulatory failure and death. The physiological mechanism underlying the induction of circulatory failure by 35-GHz microwave (MW) heating is currently unknown. The purpose of this study was to determine whether platelet-activating factor (PAF) contributes to the hypotensive state induced by MW heating. Ketamine-anesthetized rats were instrumented for the measurement of arterial blood pressure, ECG and temperature at five sites. Administration of the PAF-receptor antagonist WEB 2086 (0.5 or 5 mg/kg) following the induction of circulatory failure (defined as a decrease in mean arterial blood pressure to 75 mmHg) failed to reverse the hypotension induced by MW heating and consequently did not alter the subsequent survival time. Furthermore, pretreatment with WEB 2086 at either dose did not alter subsequent mean arterial blood pressure, temperature responses to MW heating or survival time. Finally, MW heating did not alter either blood PAF levels or serum or lung PAF acetylhydrolase levels. Taken together, these results demonstrate that PAF does not mediate the hypotension induced by 35-GHz MW heating.

Although there is no evidence that electromagnetic energy in the radio frequency radiation (RFR) band is mutagenic, there have been suggestions that RFR energy might serve as either a promoter or co-promoter in some animal models of carcinogenesis. Recent developments in electromagnetic technology have resulted in the manufacture of RFR sources capable of generating frequencies in the millimeter wave- length (MMW) range (30- 300 GHz). Because absorption of MMW energy occurs in the skin, it is to be expected that long-term detrimental health effects, if any, would most likely be manifest in the skin. In this study we investigated whether a single (1.0 W/cm2 for 10 s) or repeated (2 exposures/week for 12 weeks, 333 mW/cm2 for 10 s) exposure to 94 GHz RFR serves as a promoter or co-promoter in the 7,12-dimethylbenz[ a ]anthracene (DMBA)-induced SENCAR mouse model of skin carcinogenesis. Neither paradigm of MMW exposure significantly affected papilloma development, as evidenced by a lack of effect on tumor incidence and multiplicity. There was also no evidence that MMW exposure served as a co-promoter in DMBA-induced animals repeatedly treated with 12- O - tetradecanoylphorbol 13-acetate. Therefore, we conclude that exposure to 94 GHz RFR under these conditions does not promote or co-promote papilloma development in this animal model of skin carcinogenesis.

We examined the effect of aging on the capacity of the brain to produce heat shock protein (Hsp70) in response to heat stress, using high-powered microwaves (HPM, 2.06 GHz, 2.2 W/cm(2)) to induce hyperthermia for periods so brief that thermoregulatory factors were functionally eliminated as confounding variables. Unanesthetized young (6 months) and old (25 months) male, food-restricted Sprague-Dawley rats were exposed to HPM to induce a mean peak tympanic temperature (T(ty)) of 42.2 degrees C within 30 s. T(ty) returned to40.0 degrees C within 6 min post-exposure in both age groups. Rats were euthanized 6 or 24 h later for immunohistochemical determination of Hsp70 accumulation in 10 brain regions. HPM exposure induced significant increases in 7 of the 10 regions. There were no significant differences observed in the pattern or density of Hsp70 accumulation between the young and old rats at 6 h post-HPM exposure, with the exception of the medial vestibular nucleus, which demonstrated significantly greater Hsp70 accumulation in the old rats. There were significant differences between the age groups at 24 h post-exposure, however, there was no general pattern; i.e., depending on the brain region, aged rats displayed significantly greater, lesser, or similar increases in Hsp70 expression compared with young. Taken together, these results demonstrate that the brain of aged, food-restricted rats does not display a loss of capacity to accumulate Hsp70 in response to heat stress.

It has been suggested that chronic, low-level exposure to radiofrequency (RF) radiation may promote the formation of tumors. Previous studies, however, showed that low-level, long-term exposure of mammary tumor-prone mice to 435 MHz or 2450 MHz RF radiation did not affect the incidence of mammary tumors. In this study, we investigated the effects of exposure to a unique type of electromagnetic energy: pulses composed of an ultra-wideband (UWB) of frequencies, including those in the RF range. One hundred C3H/HeJ mice were exposed to UWB pulses (rise time 176 ps, fall time 3.5 ns, pulse width 1.9 ns, peak E-field 40 kV/m, repetition rate 1 kHz). Each animal was exposed for 2 min once a week for 12 weeks. One hundred mice were used as sham controls. There were no significant differences between groups with respect to incidence of palpated mammary tumors, latency to tumor onset, rate of tumor growth, or animal survival. Histopathological evaluations revealed no significant differences between the two groups in numbers of neoplasms in all tissues studied (lymphoreticular tissue, thymus, respiratory, digestive and urinary tracts, reproductive, mammary and endocrine systems, and skin). Our major finding was the lack of effects of UWB-pulse exposure on promotion of mammary tumors in a well-established animal model of mammary cancer.

We examined whether fatigue during exertional heat stress occurred at a critical internal temperature independent of the initial temperature at the start of exercise. Microwaves (2.1 GHz; 100 mW/cm2) were used to rapidly (3–8 min) heat rats before treadmill exercise to exhaustion. In a repeated-measures design, food-restricted male Sprague-Dawley rats ( n = 11) were preheated to three levels (low, medium, and high). In addition, two sham exposures, Sham 1 and Sham 2, were administered at the beginning and end of the study, respectively. At the initiation of exercise, hypothalamic (Thyp) and rectal (Trec) temperatures ranged from 39.0°C to 42.8°C (Thyp) and 42.1°C (Trec). The treadmill speed was 17 m/min (8° grade), and the ambient temperature during exercise was 35°C. Each treatment was separated by 3 wk. Run time to exhaustion was significantly reduced after preheating. There was a significant negative correlation between run time and initial Thyp and Trec ( r = 0.73 and 0.74, respectively). The temperatures at exhaustion were not significantly different across treatments, with a range of 41.9–42.2°C (Thyp) and 42.2–42.5°C (Trec). There were no significant differences in run time in the sham runs administered at the start and end of the investigation. No rats died as a result of exposure to any of the treatments, and body weight the day after each treatment was unaffected. These results support the concept that a critical temperature exists that limits exercise in the heat.

Sustained whole-body exposure of anesthetized rats to 35-GHz radio frequency radiation produces localized hyperthermia and hypotension, leading to circulatory failure and death. The physiological mechanism underlying the induction of circulatory failure by 35-GHz microwave (MW) heating is currently unknown. We hypothesized that oxidative stress may play a role in the pathophysiology of MW-induced circulatory failure and examined this question by probing organs for 3-nitrotyrosine (3-NT), a marker of oxidative stress. Animals exposed to low durations of MW that increased colonic temperature but were insufficient to produce hypotension showed a 5- to 12-fold increase in 3-NT accumulation in lung, liver, and plasma proteins relative to the levels observed in control rats that were not exposed to MW. 3-NT accumulation in rats exposed to MW of sufficient duration to induce circulatory shock returned to low, baseline levels. Leukocytes obtained from peripheral blood showed significant accumulation of 3-NT only at exposure levels associated with circulatory shock. 3-NT was also found in the villus tips and vasculature of intestine and within the distal tubule of the kidney but not in the irradiated skin of rats with MW-induced circulatory failure. The relationship between accumulation in liver, lung, and plasma proteins and exposure duration suggests either that nitro adducts are formed in the first 20 min of exposure and are then cleared or that synthesis of nitro adducts decreases after the first 20 min of exposure. Taken together, these findings suggest that oxidative stress occurs in many organs during MW heating. Because nitration occurs after microwave exposures that are not associated with circulatory collapse, systemic oxidative stress, as evidenced by tissue accumulation of 3-NT, is not correlated with circulatory failure in this model of shock.

Whole-body specific absorption rate (SAR) values provide useful information about energy deposition resulting from exposure to radio frequency radiation (RFR). However, whole-body SAR values do not reveal possible localized “hot spots”. Although differences in regional temperatures have been measured in animals during RFR exposure [1–3], the use of temperature probes to make empirical measurements of these “hot spots” can be extremely time consuming and are invasive in nature [4].

Specific absorption rate (SAR) is defined by the National Council on Radiation Protection and Measurements as “…the time derivative of the incremental energy absorbed by (dissipated in) an incremental mass contained in a volume of a given density” (NRCP, 1981). The whole-body and partial-body SAR form the basis of permissible exposure limits for radio frequency radiation (RFR). The whole-body SAR provides very useful information regarding the influence of frequency, polarization, and orientation on RFR absorption[1,2]. However, RFR is not absorbed uniformly throughout a biological system. Numerous factors contribute to the heterogeneity of SAR values in biological system, including differences in electrical properties of different tissues, impedance mismatches at tissue boundaries, and the complex geometry of individual organs and structures [1,2]. Due to these factors, local SAR must be used to reveal the distribution of RFR absorption within the animal. Without this information, bioeffects data obtained from one species cannot be meaningfully extrapolated to another.

Ryan, Kathy L., W. Fred Taylor, and Vernon S. Bishop.Arterial baroreflex modulation of heat-induced vasodilation in the rabbit ear. J. Appl. Physiol. 83(6): 2091–2097, 1997.—The purpose of this study was to determine whether nonthermal baroreflexes arising from cardiopulmonary and/or arterial baroreceptors modulate rabbit ear blood flow (EBF) during hyperthermia. Intact and sinoaortic-denervated (SAD) rabbits were chronically instrumented with a Doppler ultrasonic flow probe for measurement of EBF velocity (kHz). During whole body heating in conscious rabbits, EBF and ear vascular conductance (EVC) increased as core temperature increased until maximal plateau levels of EBF and EVC were reached. The maximal plateau level of EVC attained during heat stress was lower in SAD than in intact rabbits. Subsequent intrapericardial administration of procaine at maximal EBF blocked cardiac afferents but did not alter EVC in either animal group. In a second experiment, ramp decreases in mean arterial pressure were produced by vena caval occlusion at maximal EBF. In intact rabbits, EBF and EVC decreased linearly as mean arterial pressure fell, but EBF and EVC did not decrease during vena caval occlusion in SAD rabbits. Thus neither pharmacological nor mechanical unloading of cardiac baroreceptors results in reflex vasoconstriction in the heat-stressed rabbit ear. However, baroreflexes arising from arterial baroreceptors may modulate EBF in heat-stressed rabbits.

To examine the role of nitric oxide (NO) in the maintenance of working memory of rats, the effects of chronic administration (in drinking water) of the NO synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), on this behavior was examined with a simple test of remembering recently explored objects. Unlike other working memory tasks that require a subject to perform for a reward such as food or water or to avoid shock, our task measured spontaneous exploration of novel and familiar objects and has been described as a "pure" working memory task [9]. Normal subjects spend significantly more time in contact with new environmental components and less time with familiar objects. A subject that extensively reexplores a stimulus with which it has previous experience is presumed to exhibit some memory loss associated with the object. Memory changes were evaluated by measuring the relative time subjects explored familiar versus new stimulus objects. Rats (n = 15) that chronically drank L-NAME (approximately 90 mg/kg/day) for 14 days spent significantly less time exploring a novel object than did rats (n = 13) that drank only tap water (p < .05). This effect of L-NAME was abolished by concurrent administration of L-Arginine (approximately 4.5 g/kg/day). Total object exploration was not affected by our drug treatments, suggesting that our object discrimination task is not activity dependent. These data are consistent with the hypothesis that NO is required for some forms of working memory.

Over the last years, tissue microcirculatory and regional perfusion and oxygenation have made an important entry into the functional hemodynamic monitoring of critically ill patients (1). Clinical assessment of these parameters has become possible by the introduction of optical spectroscopic technologies such as near-infrared spectroscopy. This technique is based on the oxygen-dependent optical absorption of blood in the near-infrared spectrum. There are three prime factors which distinguish the currently available devices: 1) the algorithm used to calculate regional/ microcirculatory hemoglobin saturation; 2) the spatial separation of the illumination and detection fiber, which determines the measurement depth; and 3) the location of the probe. In a recent issue of Critical Care Medicine, Soller et al (2) presented a study in volunteers where a decrease in venous return (as a model of hypovolemia) was induced by lower limb negative pressure. In the model, they compared a self-developed near-infrared spectroscopy device, which measures a parameter called muscle oxygen tension, to a commercially available device from Hutchinson Technology (HT), which measures a parameter called tissue oxygen saturation and has been studied clinically (3 5). The authors concluded that their device has superior sensitivity to detect acute hypovolemia when compared with the HT device. However, in their study design, two of the above-mentioned factors were not under experimental control resulting in a faulty conclusion. This may lead to confusion in the field of those using the near-infrared spectroscopy technique and needs to be addressed.

Objective: Although linear measures of heart rate variability (HRV) (eg, RR interval high frequency, RR interval low frequency) have been associated with autonomic function, it is unclear whether nonlinear measures (ie, entropy and fractality) are similarly associated. We therefore hypothesized that nonlinear metrics of HRV would be correlated with the progressive increase in muscle sympathetic nerve activity (MSNA) induced by central hypovolemia. Methods: Twelve (7 male/5 female) healthy subjects (age, 32 ± 3 years; height, 172 ± 3 cm; weight, 80 ± 5 kg) underwent progressive lower body negative pressure (LBNP) to presyncope. Electrocardiogram and muscle sympathetic nerve activity from the peroneal nerve were measured continuously. Linear (RR interval high frequency, RR interval standard deviation, pNN50) and nonlinear (sample entropy, fractal dimensions by curve length and dispersion analysis, symbol dynamics) indices of HRV were calculated at each level of LBNP and recovery. Muscle sympathetic nerve activity was calculated as bursts per 100 heart beats (b/100 hb). Results: Muscle sympathetic nerve activity increased from 22.8 ± 2.9 b/100 hb at baseline to 46.6 ± 6.2 b/100 hb at –80 mmHg LBNP (P b .001) and returned to 21.6 ± 5.3 b/100 hb during recovery. All HRV indices decreased with LBNP and increased with recovery, resulting in inverse correlations withMSNA. The linear HRV indices were strongly correlated with MSNA (amalgamated R ≥ 0.79), whereas the only nonlinear index with an amalgamated R of 0.79 or higher was fractal dimension by dispersion analysis (R = 0.79). Conclusion: Although nonlinear indices of HRV decrease with reduced central blood volume, they are not as tightly associated with sympathetic responses as linear indices of HRV.

Medics and first responders to emergencies are often faced with monitoring and assessing victims with very limited resources. Therefore, there is an inherent need for a real-time ambulatory monitoring capability that is portable and low power. This is particularly important for physiological monitoring of life-threatening conditions such as internal hemorrhaging. We propose the use of photoplethysmogram (PPG) morphology as an indicator of hypovolemic states and study its correlation with blood pressure. In this paper, we compared the PPG morphology with pulse transit time (PTT), which has been investigated for clinical and ambulatory applications. The indicators were tested on data obtained from experiments using lower body negative pressure (LBNP) as a model to simulate hemorrhage in humans. The results of this study indicate that PPG morphology is associated with pulse pressure (systolic minus diastolic blood pressure) and is therefore a promising feature for detection and real-time tracking of hypovolemic states.