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Care of premature infants often requires parental and caregiver separation, particularly during hypoxic and hypothermic episodes. We have established a neonatal rat model of human prematurity involving maternal-neonatal separation and hypoxia with spontaneous hypothermia prevented by external heat. Adults previously exposed to these neonatal stressors show a sex difference in the insulin and glucose response to arginine stimulation suggesting a state of insulin resistance. The current study used this cohort of adult rats to evaluate insulin resistance [homeostatic model assessment of insulin resistance (HOMA-IR)], plasma adipokines (reflecting insulin resistance states), and testosterone. The major findings were that daily maternal-neonatal separation led to an increase in body weight and HOMA-IR in adult male and female rats and increased plasma leptin in adult male rats only; neither prior neonatal hypoxia (without or with body temperature control) nor neonatal hypothermia altered subsequent adult HOMA-IR or plasma adiponectin. Adult male-female differences in plasma leptin were lost with prior exposure to neonatal hypoxia or hypothermia; male-female differences in resistin were lost in the adults that were exposed to hypoxia and spontaneous hypothermia as neonates. Exposure of neonates to daily hypoxia without spontaneous hypothermia led to a decrease in plasma testosterone in adult male rats. We conclude that neonatal stressors result in subsequent adult sex-dependent increases in insulin resistance and adipokines and that our rat model of prematurity with hypoxia without hypothermia alters adult testosterone dynamics.

Peripheral immune activation can have profound physiologic and behavioral effects. One mechanism through which immune activation may affect physiology and behavior is through actions on brainstem neuromodulatory systems, such as serotonergic systems. To test this hypothesis, in Experiment 1, adult male BALB/c mice were implanted with telemetric recording devices and then immunized with Mycobacterium vaccae NCTC 11659 (0.1 mg, s.c.; Days - 28, - 14; N = 36). On Day 1, mice received an acute challenge with M. vaccae (0.1 mg, s.c.) or borate-buffered saline vehicle. Core body temperature and locomotor activity recordings were conducted during a 36 h period beginning 24 h prior to challenge; 12 h following acute challenge, mice were either tested in a 6-min forced swim test, or served as home cage controls (n = 9 per group). In Experiment 2, the protocol was repeated, but with the aim of assessing c-Fos expression in brainstem serotonergic neurons, assessed 90 min following exposure to forced swim (N = 32; n = 8 per group). In Experiment 1, acute M. vaccae challenge in M. vaccae-immunized mice, relative to vehicle-challenged controls, decreased locomotor activity and core body temperature measured 3 h following challenge, as measured by continuous telemetric recordings, and decreased immobility in the forced swim test measured 12 h following challenge. In Experiment 2, acute M. vaccae challenge in M. vaccae-immunized mice decreased home cage locomotion, in alignment with findings in Experiment 1, as measured by video-based behavioral analysis, and, among mice exposed to the forced swim test, increased c-Fos expression in subsets of serotonergic neurons within the dorsal raphe nucleus (DR) measured 13.5 h following challenge. Together, these data are consistent with the hypothesis that acute peripheral immune activation with a heat-killed preparation of M. vaccae transiently induces mild hypothermia in association with suppression of locomotor activity, activates subsets of serotonergic neurons in the DR, and induces antidepressant-like behavioral responses.

Purpose: To report a case of hypothermia in a patient with intellectual disability treated with thioridazine., Summary: A 59-year-old female presented to the emergency department with altered mental status, generalized weakness, chills, and fatigue and was diagnosed with a urinary tract infection. Upon completion of a history and physical examination, the patient was found to be hypothermic with a temperature of 91 F. A Bair Hugger protocol was initiated to manage hypothermia, and a taper schedule for thioridazine was initiated as it was identified as a possible culprit for the patient's hypothermia. According to the Naranjo probability scale, thioridazine was a possible cause of this adverse effect. Other patient-specific risk factors for hypothermia were evaluated and ruled out., Conclusion: This case indicates a possible correlation between hypothermia and the use of phenothiazine antipsychotics such as thioridazine. Appropriate measures, including early detection and identification of possible causative agents, should be taken to prevent and treat this adverse event in patients taking these medications, specifically in patients with the inability to participate in self-care., (© The Author(s) 2016.)

Parental behavioural traits can be transmitted by non-genetic mechanisms to the offspring. Although trait transmission via sperm has been extensively researched, epidemiological studies indicate the exclusive/prominent maternal transmission of many non-genetic traits. Since maternal conditions impact the offspring during gametogenesis and through fetal/early-postnatal life, the resultant phenotype is likely the aggregate of consecutive germline and somatic effects; a concept that has not been previously studied. Here, we dissected a complex maternally transmitted phenotype, reminiscent of comorbid generalized anxiety/depression, to elementary behaviours/domains and their transmission mechanisms in mice. We show that four anxiety/stress-reactive traits are transmitted via independent iterative-somatic and gametic epigenetic mechanisms across multiple generations. Somatic/gametic transmission alters DNA methylation at enhancers within synaptic genes whose functions can be linked to the behavioural traits. Traits have generation-dependent penetrance and sex specificity resulting in pleiotropy. A transmission-pathway-based concept can refine current inheritance models of psychiatric diseases and facilitate the development of better animal models and new therapeutic approaches.

Alzheimer's disease (AD) is a primary neurodegenerative disorder associated with progressive memory impairment. Recent studies suggest that hypothermia may contribute to the development and exacerbation of AD. The aim of this study was to investigate the role of chronic hypothermia on spatial learning and memory performance as well as brain immunohistochemical (IHC) and molecular changes. Four groups of male rats were placed in cold water (3.5 ± 0.5 °C) once a day for 1, 3, 6, and 14 days, four other groups were placed in warm water (32 °C) as the control groups to eliminate the effect of swimming stress, and one more group which comprised intact animals that were kept in a normothermic situation and had no swimming stress. Twenty-four hours after the last intervention, spatial learning and memory were assessed, using the modified Morris water maze. After the behavioral test, the rats' brains were removed for IHC and Western blotting. The results showed that memory retrieval is impaired after 14 days of cold water-induced hypothermia (CWH) (P < 0.05). IHC showed the formation of beta-amyloid plaques after a 14-day CWH. The molecular changes demonstrated that a 14-day CWH induces tau hyperphosphorylation, apoptosis, and reduces COX-II expression. Therefore, chronic CWH, independent of forced swimming stress, impairs learning and memory through molecular mechanisms similar to those of AD. In conclusion, CWH may serve as an important model to assess the role of hypothermia in AD pathogenesis.

Male BALB/c mice single-housed for a period of three weeks were found to respond with a more marked hypothermia to a challenge with a selective serotonergic agonist (8-OH-DPAT) than their group-housed counterparts. This effect of single housing was verified by screening a genetically heterogeneous population of male mice on a C57BL/6 background from a breeding colony. Enhanced activity of the implicated receptor (5-HT1A) leading to an amplified hypothermic effect is strongly associated with depressive states. We therefore suggest that the 8-OH-DPAT challenge can be used to demonstrate a negative emotional state brought on by e.g. long-term single housing in male laboratory mice. The study emphasizes the importance of social housing, and demonstrates that male mice deprived of social contact respond with altered serotonergic signaling activity. Male mice not only choose social contact when given the option, as has previously been shown, but will also, when it is deprived, be negatively affected by its absence. We propose that the 8-OH-DPAT challenge constitutes a simple, but powerful, tool capable of manifesting the effect of social deprivation in laboratory mice. It potentially allows not only for an unbiased, biochemical evaluation of psychological stressors, but may also allow for determining whether the effect of these can be counteracted.

The circadian system develops and changes in a gradual and programmed process over the lifespan. Early in life, maternal care represents an important zeitgeber and thus contributes to the development of circadian rhythmicity. Exposure to early life stress may affect circadian processes and induce a latent circadian disturbance evident after exposure to later life stress. Disturbance of the normal regulation of circadian rhythmicity is surmised to be an etiological factor in depression. We used postnatal maternal separation in rats to investigate how the early life environment might modify the circadian response to later life unpredictable and chronic stress. During postnatal days 2-14, male Wistar rats (n = 8 per group) were daily separated from their mothers for a period of either 180 min (long maternal separation; LMS) or 10 min (brief maternal separation; BMS). In adulthood, rats were exposed to chronic mild stress (CMS) for 4 weeks. Body temperature, locomotor activity and heart rate were measured and compared before and after CMS exposure. LMS offspring showed a delayed body temperature acrophase compared to BMS offspring. Otherwise, adult LMS and BMS offspring demonstrated similar diurnal rhythms of body temperature, locomotor activity and heart rate. Exposure to CMS provoked a stronger and longer lasting hypothermia in LMS rats than in BMS rats. The thermoregulatory response appears to be moderated by maternal care following reunion, an observation made in the LMS group only. The results show that early life stress (LMS) in an early developmental stage induced a thermoregulatory disturbance evident upon exposure to unpredictable adult life stressors.

Using a retrograde amnesia procedure, the susceptibility of the extinction of fear conditioning was assessed in two experiments. Extinction of a passive-avoidance task was impaired by a body-cooling treatment (e.g., hypothermia; [7]) which was too mild to induce amnesia for the avoidance training, suggesting that the memory for extinction is more susceptible to body cooling than the memory for the initial fear conditioning. Decreasing the severity of the treatment decreased its ability to disrupt extinction. Thus, the study demonstrates a difference in the vulnerability to amnesia of fear conditioning vs. extinction of that fear., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Background: Patients in prehospital care, irrespective of diseases or trauma might experience thermal discomfort because of a cold environment and are at risk for decreasing body temperature which can increase both morbidity and mortality., Objective: To explore patients' experiences of being cold when injured in a cold environment., Method: Twenty persons who had been injured in a cold environment in northern Sweden were interviewed. Active heat supply was given to 13 of them and seven had passive heat supply. The participants were asked to narrate their individual experience of cold and the pre- and post-injury event, until arrival at the emergency department. The interviews were transcribed verbatim, then analyzed with qualitative content analysis., Results: Patients described that they suffered more from the cold than because of the pain from the injury. Patients who received active heat supply experienced it in a positive way. Two categories were formulated: Enduring suffering and Relief of suffering., Conclusion: Thermal discomfort became the largest problem independent of the severity of the injuries. We recommend the use of active heat supply to reduce the negative experiences of thermal discomfort when a person is injured in a cold environment., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

This example of a fatal diving accident shows how challenging such cases can be in pre-hospital and clinical care. There is no common mechanism in diving fatalities and more than one group of disorders coming along with decompression sickness. Diving medicine is not an element of medical education, which results in insecurity and hampers adequate therapy of diving incidents. This is aggravated by an insufficient availability of hyperbaric chambers in Germany.

A number of drugs and psychological stressors induce brain hyperthermia and increase extracellular dopamine in the caudate-putamen. The present study tested whether caudate-putamen hyperthermia produced by such stimuli is dependent on dopaminergic transmission. Rats were infused with 6-hydroxydopamine unilaterally into the medial forebrain bundle, and after a two-week recovery period, removable thermocouples were used to monitor temperature in the depleted and intact caudate-putamen in freely-moving animals. The indirect dopamine agonist d-amphetamine (1 and 2mg/kg s.c.) increased caudate-putamen temperature, whereas a low dose of the direct agonist apomorphine (0.1mg/kg s.c.) reduced it. Gamma-butyrolactone, which strongly inhibits dopamine release at the dose administered (700mg/kg i.p.), initially reduced and then increased caudate-putamen temperature. Brief (5-10min) presentation of mild stressors, including tail pinch, produced a rapid and transient caudate-putamen hyperthermia. Quantitative (125)I-RTI-55 autoradiography in post-mortem tissue revealed a 97-100% loss of binding to dopamine transporters in the lesioned caudate-putamen. Despite this near-total dopamine denervation, neither basal caudate-putamen temperature, nor any of the observed temperature responses to drugs or mild stressors, was altered. We conclude that in the caudate-putamen, endogenous dopamine is unlikely to modulate temperature significantly at a local level., (Copyright 2010 Elsevier Inc. All rights reserved.)

Aging is a consequence of progressive decline in special and somatosensory functions and specific brain stem nuclei. Many senescent stigmata, including hypoxia, hypoxemia, depressed cerebral blood flow and glucose metabolism, diseases of senescence, and their medications all enhance hypothermia as do alcohol, cold environment, and malnutrition. Hypothermia is a critical factor having deleterious impact on brain stem and neocortical functions. Additionally, anesthesia in elderly also promotes hypothermia; anesthetics not only cause consciousness (sensory and motor) changes, but memory impairment as well. Anesthesia inhibits cholinergic pathways, reticular and thalamocortical systems, cortico-cortical connectivity, and causes post-operative delirium and cognitive dysfunction. Increasing evidence indicates that anesthetic exposures may contribute to dementia onset and Alzheimer's disease (AD) in hypothermic elderly. Inhaled anesthetics potentiate caspases, BACE, tau hyperphosphorylation, and apoptosis. This paper addresses the important question: "Why do only some elderly fall victim to AD"? Based on information on the pathogenesis of early stages of cognitive dysfunction in elderly (i.e., due to senescent stigmata), and the effects of anesthesia superimposed, a detailed plausible neuropathological substrate (mechanism/pathway) is delineated here that reveals the possible cause(s) of AD. Basically, it encompasses several risk factors for cognitive dysfunction during senescence plus several hypothermia-enhancing routes; they all converge and tip the balance towards dementia onset. This knowledge of the confluence of heterogeneous risk factors in perpetuating dementia relentlessly is of importance in order to: (a) avoid their convergence; (b) take measures to stop/reverse cognitive dysfunction; and (c) to develop therapeutic strategies to enhance cognitive function and attenuate AD.

Memory consolidation is the process by which new and labile information is stabilized as long-term memory. Consolidation of spatial memories is thought to involve the transfer of information from the hippocampus to cortical regions. While the hypometabolic and hypothermic state of torpor dramatically changes hippocampal connectivity, little work has considered the functional consequences of these changes. The present study examines the role of a single bout of shallow torpor in the process of memory consolidation in mice. Adult female C57Bl/6NHSD mice were trained on the Morris Water Maze (MWM) task. Immediately following acquisition, the mice were exposed to one of four experimental manipulations for 24 h: fasted at an ambient temperature of 19 degrees C, fasted at 29 degrees C, allowed free access to food at 19 degrees C, or allowed free access to food at 29 degrees C. Mice fasted at 19 degrees C entered a bout of torpor as assessed by core body temperature while none of the mice in the other conditions did so. Spatial biases were then assessed with a probe trial in the MWM. During the probe trial, mice that had entered torpor and mice that were fed at 29 degrees C spent twice as much time in the prior target platform location than mice that were fed at 19 degrees C and those that were fasted at 29 degrees C. These findings demonstrate that, while food restriction or cool ambient temperature independently disrupt memory processes, together they cause physiological changes including the induction of a state of torpor that result in functional preservation of the memory process.

Objectives: Cold water temperature is a significant factor in North American drownings. These deaths are usually attributed to hypothermia. Survey questions were administered to 661 attendees of cold-stress seminars-including medical, rescue, law enforcement and lay attendees-to determine general knowledge of the effects of ice water immersion and responses to 2 public service educational slogans., Methods: Five questions were posed at the beginning of seminars to 8 groups (ranging in size from 46 to 195) during a 2-year period. Pi(2) analyses were used to determine if responses within any occupational category differed from the group responses., Results: A high portion of respondents greatly underestimated the time to become hypothermic in ice water (correct answer >30 minutes; 84% stated 15 minutes or less) and the time until cooling was life threatening (correct answer >60 minutes; 85% stated 30 minutes or less). There were no occupational differences in these responses. Most of the respondents identified a correct cause of death during cold stress (81% stated cardiac arrest, hypothermia, or drowning). Although both educational slogans had some advantages, between 40% (Slogan #1) to 50% (Slogan #2) of respondents did not respond correctly., Conclusions: The majority of respondents underestimated the time available for survival during ice water immersion. It is important to educate the public accurately to decrease the probability of panic under these circumstances. More work is required to develop effective educational slogans that provide proper information and actions for victims of cold-water immersion.

The effects of hypothermia on memory formation have been examined extensively, and while it is clear that post-training cooling interferes with the process of consolidation, the nature of the temperature sensitive processes disrupted in this way remain poorly defined. Post-training manipulations that disrupt consolidation tend to be effective during specific time-windows of sensitivity, the timing and duration of which are directly related to the mechanism through which the treatment induces amnesia. As such, different treatments that target the same basic processes should be associated with similar time-windows of sensitivity. Using this rationale we have investigated the possibility that cooling induced blockade of long-term memory (LTM) stems from the disruption of protein synthesis. By varying the timing of post-training hypothermia we have determined the critical period during which cooling disrupts the consolidation of appetitive long-term memory in the pond snail Lymnaea. Post-training hypothermia was found to disrupt LTM only when applied immediately after conditioning, while delaying the treatment by 10 min left the 24 h memory trace intact. This brief (<10 min) window of sensitivity differs from the time-window we have previously described for the protein synthesis inhibitor anisomycin, which was effective during at least the first 30 min after conditioning [Fulton, D., Kemenes, I., Andrew, R. J., & Benjamin, P. R. (2005). A single time-window for protein synthesis-dependent long-term memory formation after one-trial appetitive conditioning. European Journal of Neuroscience, 21, 1347-1358]. We conclude that hypothermia and protein synthesis inhibition exhibit distinct time-windows of effectiveness in Lymnaea, a fact that is inconsistent with the hypothesis that cooling induced amnesia occurs through the direct disruption of macromolecular synthesis.

Two men, 56 and 33 years old, (case 1 and case 2) were examined neuropsychologically after successful resuscitation from circulatory arrest following extreme accidental hypothermia and near drowning. After submersion in ice water for at least 20 minutes they received CPR for 45 to 60 minutes. Body-core temperature at start of CPB was 24 degrees C and 22 degrees C, respectively. A neuropsychological examination was performed within two months after the accident and 1 year later. An additional follow-up interview was made 3 years after the accidents. Both had severe problems with memory, visuospatial performance, executive function, and verbal fluency. The follow-up demonstrated improvement in the visuospatial test in both and in the verbal learning, recall, and logical reasoning tests in case 2. Both still had problems with executive function, and case 2 also in verbal fluency. Case 1 also had problems with flexibility, planning and abstract ability. Despite the protective effects of hypothermia and gradual improvement of symptoms over time, some of the deficits were permanent. A thorough neuropsychological examination of patients suffered from anoxia is advisable, because gross neurological examination and MRI scans may not always reveal underlying brain dysfunction.

Regulations of hormonal stress responses entail the initiation, amplitude and termination of the reaction, as well as its integration with other stress response systems. This study investigates the role of endogenous opioids in the regulation and integration of behavioral, thermal and hormonal stress responses, as these neuromodulators and their receptors are expressed in limbic structures responsible for stress responses. For this purpose, we subjected mice with selective deletion of beta-endorphin, enkephalin or dynorphin to the zero-maze test, a mildly stressful situation, and registered behaviors and stress hormone levels. Behavioral stress reactivity was assessed using zero-maze, light-dark and startle-reactivity paradigms. Animals lacking enkephalin displayed increased anxiety-related behavioral responses in each three, dynorphin knockouts in two models, whereas the responses of beta-endorphin knockouts indicated lower anxiety level in the zero-maze test. All knockout strains showed marked changes in hormonal stress reactivity. Increase in ACTH level after zero-maze test situation, unlike in wild type animals, failed to reach the level of significance in Penk1(-/-) and Pdyn(-/-) mice. Corticosterone plasma levels rapidly increased in all strains, with a lower peak response in knockouts. In wild-type and beta-endorphin-deficient mice, corticosterone levels returned to baseline within 60min after stress exposure. In contrast, mice lacking dynorphin and enkephalin showed longer-lasting elevated corticosterone levels, indicating a delayed termination of the stress reaction. Importantly, the behavioral and hormonal responses correlated in wild-type but not in knockout mice. Hyperthermia elicited by stress was reduced in animals lacking dynorphin and absent in Penk1(-/-) mice, despite of the heightened behavioral anxiety level of these strains. These results demonstrate an important role on the endogenous opioid system in the integration of behavioral and hormonal stress responses.

Children with severe neurodevelopmental impairment are at risk for recurrent hypothermia, defined as a temperature of less than 35 degrees C, as a result of hypothalamic dysfunction. Acute pancreatitis following hypothermia from environmental exposure or induced as medical therapy has been reported in adults. In this case series of 10 children (six males, four females) with severe neurodevelopmental impairment and associated hypothermia, five had an episode of acute pancreatitis. These five patients had documented hypothermia, an elevated lipase of greater than 1000U/L, and presenting symptoms of irritability or lethargy along with gastrointestinal symptoms such as feeding intolerance. Four of these five children had no other explanation for pancreatitis; the fifth had multiple gallstones. This case series identifies the risk of acute pancreatitis in children with central hypothermia. Monitoring for resolution upon establishment of euthermia can minimize unnecessary testing and cost.

Introduction: This study evaluated performance after lowering core temperature at different rates while local tissues were either cooled (lower body) or not cooled (upper body)., Methods: There were 10 men who volunteered to perform up to 8 cold water immersions (CWI) at combinations of 2 water temperatures (10 degrees C and 15 degrees C), 2 depths [waist (W), chest (C)], and 2 walking speeds (0.44 or 0.88 m x s(-1)) until their core temperature fell to 35.5 degrees C, stabilized above that temperature, or they requested to stop. They also completed a control trial (120 min rest in 19 degrees C air). Immediately following each CWI and control, cognitive and physical performance tests were performed in cold air (10 degrees C; CAE)., Results: Overall, the CWI protocol lowered rectal temperature by 0.3-1.0 degrees C. Mean skin temperature was approximately 26 degrees C and finger temperature was approximately 15 degrees C during CAE. No statistical differences were observed across trials for any cognitive test. On the physical performance tests, step test performance was degraded approximately 12% on CWI trials compared with control, but there were no differences in manual dexterity, hand grip strength, marksmanship, or pull-ups., Conclusions: These results indicate that cognitive performance can be maintained despite mild hypothermia, and that physical performance is related to local tissue temperature, not a moderately reduced core temperature.

Behavioral immobility during forced swim is usually considered a consequence of inescapable stress, and is used to screen antidepressant drugs. However, immobility in this test may also result from inhibition of neural functions because of brain hypothermia due to body cooling. To explore this possibility, we measured brain temperature dynamics during a 10-min forced swim in cold (25 degrees C) and warm (37 degrees C) water and correlated brain temperatures with behavioral changes. Cold water forced swim resulted in significant brain hypothermia (-6-7 degrees C) and immobility, while no immobility was observed during warm water forced swim, when brain temperature transiently increased (0.5 degrees C) then decreased below baseline in the post-swim period. These data suggest that immobility, which rapidly develops during forced swim in cold water, may result from dramatic inhibition of neural functions because of severe brain hypothermia.

The Morris water maze, one of the most common behavioral tasks to assess learning and memory in rodents, exposes the animals to cold water for a few minutes. Unlike rats, young healthy mice can become severely hypothermic during the task. Five swims of 45 s in 20 degrees C water with 30s between the trials was enough to cause up to 9 degrees C drop in the rectal temperature. The decline in core temperature was accompanied by slowing of the swimming speed. Moreover, the effect was dependent on the sex and genotype of the mice, such that females were more susceptible to hypothermia than males and transgenic mice carrying Alzheimer-associated APP and PS1 mutations more vulnerable than their nontransgenic littermates. Raising the water temperature from 20 to 24 degrees C alleviated the hypothermia, but did not remove the significant drop in core temperature when using 30-s inter-trial interval. However, increasing the break from 30 s to 13 min removed the net cooling effect of five trials on the core temperature and swimming speed. We conclude that the currently most common water maze protocol renders mice hypothermic, which may confound the test results, especially when transgenic female mice are used. We recommend monitoring of the swimming speed on a trial-by-trial basis and using longer inter-trial intervals.

Swiss-Webster mice selectively bred for high swim stress-induced analgesia (SSIA) were exposed to continuous ambient cold (5 degrees C) for 6 weeks or to daily 3-min swims for 14 consecutive days either in 20 or 32 degrees C water. Thereafter, mice subjected to the particular procedure were injected intraperitoneally with 10 mg/kg of naltrexone HCl and were tested for modification of the opioid and nonopioid component of SSIA. SSIA was reduced following swims at either water temperature and was antagonized by naltrexone to greater extent than in nonswimming mice. Thus, the nonopioid (i.e. naltrexone-resistant) portion of the overall SSIA was significantly reduced, whereas the opioid (naltrexone-sensitive) portion became relatively augmented. In contrast, SSIA differed neither in magnitude nor in sensitivity to naltrexone between cold-acclimated and unacclimated mice. Swim hypothermia as well as the nonopioid component of SSIA were decreased after repeated swimming at 32 and 20 degrees C, but remained unchanged after cold acclimation. This argues for the essential role of an extrathermal, probably emotional in nature, factor not only in the elicitation of nonopioid SSIA, but also in the modulation of thermoregulatory processes during swimming. We suggest that the emergency component of swim stress, together with initial moderate hypothermic challenge, first produces the opioid form of SSIA, and subsequently, as the swim continues, also affects the thermoregulatory processes maintaining thermal homeostasis. This causes further increase in swim hypothermia and raises its stressing property to induce the nonopioid form of SSIA.

Rationale: Animals prenatally exposed to ethanol (ethanol-exposed animals) exhibit physiological and behavioral abnormalities consistent with altered 5-hyrdroxytryptamine (5-HT) function including lack of response inhibition and increased anxiety and aggression., Objective: The present study investigated the possibility that ethanol-exposed animals show alterations in 5-HT(1A) and 5-HT(2A) receptor function, two 5-HT receptor subtypes mediating these behaviors. We measured the physiological and behavioral responses to the 5-HT(1A) agonist 8-hydroxy-2-(di- n-propylamino)tetralin (8-OH-DPAT), and the 5-HT(2A/C)agonist (+/-)-1-(2, 5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride) (DOI), which provide indices for estimating central changes in 5-HT activity and receptor function., Methods: Female and male offspring from ethanol-exposed (E), pair-fed control (PF), and ad-libitum-fed control (C) dams were tested in adulthood. Animals were injected with 8-OH-DPAT or DOI to induce hypothermia and wet-dog shakes (WDS, a paroxysmal shudder of the head, neck and trunk), respectively, or with saline. In experiment 1, core temperatures were recorded immediately before injection of 8-OH-DPAT (0, 0.125 mg/kg or 0.500 mg/kg) and again at 30, 60, 90, 120 and 180 min post-injection. In experiment 2, the number of WDS were recorded in response to injection of DOI (0, 1 mg/kg)., Results: E females and males showed a greater hypothermic response to 8-OH-DPAT than PF and C animals. E females and males also showed less of a differential hypothermic response to low and high doses of 8-OH-DPAT than PF and C animals. In addition, in response to DOI, E females, but not males, showed a significantly greater rate of WDS than PF and C females., Conclusions: Our findings indicate that prenatal ethanol exposure alters 5-HT(1A) and 5-HT(2A) receptor function in adulthood and does so in a sex-specific manner. These findings have important implications for altered hormonal and behavioral responsiveness observed in ethanol-exposed animals.

Previous research has demonstrated that repeated exposure to cold water results in cold tolerance. The present set of experiments examined whether spontaneous behavioral activity and the rate of rewarming differed between cold tolerant and nontolerant rats. Animals receiving six cold exposures (one per day) were compared to subjects receiving a single cold exposure but cooled to match the final day temperature of the six-exposure group. Immediately following the final or only cold exposure, activity was measured by an activity monitor (Exp. 1) or was videotaped and scored by an independent observer (Exp. 2). Furthermore, rats' temperatures were monitored for 90 min (Exp. 2) and 60 min (Exp. 3) following the activity measurement. The results indicated that cold-tolerant rats exhibited activity similar to normal, noncooled subjects, whereas the activity in the single exposure group was impeded. Moreover, rats in the multiple exposure groups rewarmed more quickly than subjects in the single exposure condition. The third experiment also examined if the procedures of Experiments 1 and 2 resulted in associative cold tolerance. Experiment 3 replicated earlier findings, which have shown that exposure to the same cold stimulus in an altered context resulted in a loss of tolerance. These findings suggest that the processing of contextual stimuli is necessary for the acquisition of cold tolerance and that behavioral activity and rewarming rates can be used as alternative measures of cold tolerance.

A case of self-inflicted bite injuries of the fingers with an episode of small intracerebral haemorrhages is presented. There were many injuries on the right fingers. The tip of the right forefinger was bitten off, and some small pieces of the finger had been aspirated and swallowed. This unusual case seemed to be an emotional response to pain from cerebral episode.

A 31-yr-old woman demonstrated intact neuropsychological functioning after being submerged for at least 30 minutes in icy cold water. Following submersion, the patient received CPR for approximately 1 hr. Eight hours after submersion, the patient's temperature was 31 degrees C (87 degrees F). She remained nonresponsive for 2 days after the accident. Extensive neuropsychological testing was completed 3 mo after the accident with no objective or subjective deficits evidenced. This case of hypothermically mediated neuroprotection from anoxia in an adult supports the need for further research on the putative neurophysiological mechanisms invoked and the potential for application of clinically induced hypothermia in the acute management of other types of cerebral insults.

The effect of task complexity on the decrement in mental performance during immersion hypothermia was studied. Psychometric tests of varying length and complexity were administered: 1) prior to cold water immersion (baseline); 2) soon after immersion to the neck in cold (8 degrees C) water but prior to any decrease in core temperature; and 3) after 55 to 80 min of immersion when core temperature had decreased 2-4 degrees C. Results indicated that tests placing relatively minimal cognitive demands on individuals, such as auditory attention, the Benton visual recognition test and forward digit span, were unaffected by either initial cold water immersion or central cooling. On the other hand, tests requiring relatively greater mental manipulation and short term memory (i.e., backward digit span) or processing and analysis (i.e., Stroop test) showed a slight improvement upon cold water immersion (perhaps related to increased arousal and/or learning) but a significant decrement following central cooling of 2-4 degrees C. Thus, relatively simple tasks were unaffected by central cooling, whereas more complex tasks were adversely affected. Cold water immersion itself did not interfere with performance of any tasks. Central nervous system cooling probably interferes with mental processing although discomfort and/or the physiological and physical effects of cold on the neuromuscular aspects of speech, required for responses to some of the tasks, may also affect performance.

Cold injured patients in Alaska come from many sources. Although sport and work continues to provide large numbers of cold injured, most severe repeat injuries tend to reflect other biopsychosocial consequences. Certain behaviors can increase the probability of injury, however all persons living in cold climates are potential candidates. One can decrease risk by education, knowledge and intelligent behavior. Proper respect for adequate protection and hydration seem to be critical factors. Understanding the psychological, physiological and psychophysiological aspects of the cold environment performer helps refine the prevention and treatment strategies for cold injury. Skill training with bio-behavioral methods, such as thermal biofeedback, and the value of medical psychotherapy appear to offer continued promise by facilitating physiologic recovery from injury, as well as assisting in long term rehabilitation. Both approaches increase the likelihood of a favorable healing response by soliciting active patient participation. Medical Psychotherapy for traumatic injuries can also help identify and manage cognitive emotional issues for families and patients faced with the permanent consequences of severe thermal injuries. Thermal biofeedback therapy has the potential benefit of encouraging greater self-reliance and responsibility for self-regulating overall health by integrating self-management skills regarding physiology, diet and lifestyle. Inpatient and outpatient biofeedback training offers specific influence over vascular responses for healing, as well as providing an effective tool for pain management. Interest in cold region habitation has continued to expand our study of human tolerance to harsh, extreme environments. Biological, psychological, sociological, and anthropological views on adaptation, habituation, acclimatization, and injury in cold environments acknowledges the role of development, learning and educated responses to cold environments. The study of health, performance, and injury prevention in extreme isolated cold environments has important strategic and scientific implications. What is learned from behavioral studies of cold survival provides an opportunity to increase our scientific knowledge and understanding. These cold research findings can assist in our future exploration of cold, underwater farming at great depths, and to far distance space travel to cold planets. The relatively new research frontier "Polar Psychology" has evolved to study how interactions with cold environments can have both positive and/or negative consequences. This research simulates the psychological factors likely to be encountered while exploring isolated cold regions of distant galaxies. The psychological and psychophysiological correlates of cold experience appear to be a function of four interactive issues: the environment, genetic predisposition, learning or experience, and finally perception or cognition. Individual cold tolerance seems to relate heavily on sensation, perception and behavior.(ABSTRACT TRUNCATED AT 400 WORDS)

This study tested the hypothesis that ethanol intake and preference for ethanol-paired flavors are inversely related to the magnitude of hypothermia induced by ethanol. Fluid-deprived rats were given 15-min daily access to 7% ethanol in one of two flavored saccharin solutions. Consumption of one flavored ethanol solution (counterbalanced) was consistently followed by 6-hr placement in a room maintained at 32 degrees C, whereas, consumption of the other flavored ethanol solution was followed by maintenance at room temperature (21 degrees C). Animals experienced less hypothermia when ethanol was followed by exposure to 32 degrees C and eventually drank more of the flavored ethanol that preceded this exposure. Moreover, intermittent two-bottle choice tests revealed development of a preference for the flavor that preceded exposure to 32 degrees C. An "extinction" phase indicated that this preference was not due to association with the thermal environments, but depended on differences in ethanol-induced hypothermia. These results support the conclusion that oral intake of ethanol is modulated by ethanol-induced hypothermia, most likely through a conditioned taste aversion mechanism.

The phenomenon called paradoxical undressing has been described from 33 cases of hypothermia collected from Swedish police reports. The cases were almost evenly distributed with regard to sex, age, and geographical distribution. The cases occurred more frequently in open land although cases from town areas were also found. Most incidents were recorded from November to February at low ambient temperatures, although cases were also reported at temperatures above 0 degree C. Arteriosclerosis and chronic alcoholism were important concomitant illnesses, the latter being frequent in middle-aged men. Epilepsy, diabetes, and pregnancy were present in single cases. Ethanol and other drugs were present in 67% of the males and in 78% of the females, ethanol predominating in men and various psychotropic agents in women. The mean blood ethanol concentration in males was 0.16% and in females, 0.18%. Most frequent findings at necropsy were purple spots or discoloration on the extremities, pulmonary edema, and gastric hemorrhages. It is concluded that paradoxical undressing might be explained by changes in peripheral vasoconstriction in the deeply hypothermic person. It represents the last effort of the victim and is followed almost immediately by unconsciousness and death.