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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 1.0, 3.0 and 5.0 g/kg of ethanol on blood glucose levels and body temperature were examined in rats submitted to either acute food deprivation (24 or 48 hr), chronic starvation, or to both chronic plus acute food deprivation. The results show that: (a) 3.0 and 5.0 g/kg produced either an increase or a decrease of glucose levels depending on the state of fasting; (b) rats not deprived of food presented hyperglycemia while being hypothermic; (c) a marked hypothermia was present when no substantial alterations in glycemia were observed; and (d) in cases where hypoglycemia and hypothermia occurred, the fall in body temperature paralleled or preceded the decrease in glucose levels.
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PMID:Blood glucose and body temperature alterations induced by ethanol in rats submitted to different levels of food deprivation. 729 Dec 58

The peak time period for the average beef producer to experience the majority of calf losses has consistently been from the time of birth through the first seven days of life. Weakness is a principal clinical sign of diseases or conditions responsible for mortality including birth trauma, prematurity or dysmaturity, congenital malformations, metabolic defects, intrauterine infection, anoxia or hypoxia, hypothermia, starvation, extremes in birth weight, and post-natal infection. This article discusses anoxia/hypoxia and septicemia in greater detail because of their involvement as a common cause of weakness in the newborn calf.
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PMID:Weakness in the newborn calf. 819 20

The purpose of this study was to determine if the ketone body beta-hydroxybutyrate (beta-HBA) is a useful positive marker for sudden deaths in chronic alcoholics, thought to be due to hypoglycemia. Beta-HBA can be reliably measured in postmortem samples of vitreous humour and urine. In fatalities where there is a history of chronic alcoholism and routine investigations, including autopsy and routine toxicology, yield only a fatty liver as positive findings, a raised level of beta-HBA can be used as an indicator for alcoholic ketosis. Alcoholic ketosis is often associated with antemortem hypoglycemia. Caution should be observed in attributing the significance of ketosis exclusively to alcohol in those conditions where it would otherwise be expected (i.e. diabetic ketoacidosis and chronic starvation). A measurement of this marker of alcoholic ketosis may also help in the investigation of cases where hypothermia or alcohol withdrawal fits are suspected.
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PMID:The investigation of beta-hydroxybutyrate as a marker for sudden death due to hypoglycemia in alcoholics. 830 32

Reports of the effect of desynchronized sleep (DS) deprivation on body temperature (Tb) of rats in the literature are contradictory. Since conspicuous body weight loss is common in such deprivation, the effect of food plus DS deprivation on Tb of adult male Wistar rats was studied. DS deprivation carried out by the small platform method with food ad libitum (N = 8) induced hyperthermia (Tb above 38.5 degrees C) in 1 to 3 rats daily until the 8th day, when a case of discrete hypothermia (Tb below 36.9 degrees C) appeared. Food deprivation alone started to induce hypothermia on the third day in one (20%) out of five rats. Fasting imposed from the 5th to the 8th day of DS deprivation (N = 12) caused hypothermia in 33% and 67% of the animals on the second and third day of starvation, respectively. DS compensatory manifestations in 6 starved rats intensified (N = 2) or precipitated (N = 2) hypothermia after the end of sleep deprivation. It is concluded that the hypothermia is not a primary effect of DS deprivation, and this state of sleep seems to have its particular functional role which is independent of thermoregulation.
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PMID:Food deprivation and hypothermia in desynchronized sleep-deprived rats. 873 30

Norepinephrine and its metabolites were studied in various body fluids (plasma, urine and cerebrospinal fluid) of patients with anorexia nervosa, bulimia nervosa and healthy young women. The reaction of plasma norepinephrine to different stimuli like orthostatic challenge, test meals, standardized exercise, mental challenge tests etc. were studied. All results indicate a reduced noradrenergic activity in the central and peripheral nervous system of patients with eating disorders. The clinical consequences of these changes are hypotension, bradicardia, hypothermia and depression. Evidence is presented that the reduced activity of the sympathetic nervous system is caused by starvation (anorexia nervosa) or intermittent dieting (bulimia nervosa).
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PMID:Central and peripheral noradrenalin regulation in eating disorders. 873 14

In addition to the well-documented seasonal cycles of mating and birth, there are also significant seasonal cycles of illness and death among many animal populations. Challenging winter conditions (i.e., low ambient temperature and decreased food availability) can directly induce death via hypothermia, starvation, or shock. Coping with these challenges can also indirectly increase morbidity and mortality by increasing glucocorticoid secretion, which can compromise immune function. Many environmental challenges are recurrent and thus predictable; animals could enhance survival, and presumably increase fitness, if they could anticipate immunologically challenging conditions in order to cope with these seasonal threats to health. The annual cycle of changing photoperiod provides an accurate indicator of time of year and thus allows immunological adjustments prior to the deterioration of conditions. Pineal melatonin codes day length information. Short day lengths enhance several aspects of immune function in laboratory studies, and melatonin appears to mediate many of the enhanced immunological effects of photoperiod. Generally, field studies report compromised immune function during the short days of autumn and winter. The conflict between laboratory and field data is addressed with a multifactor approach. The evidence for seasonal fluctuations in lymphatic tissue size and structure, as well as immune function and disease processes, is reviewed. The role of pineal melatonin and the hormones regulated by melatonin is discussed from an evolutionary and adaptive functional perspective. Finally, the clinically significance of seasonal fluctuations in immune function is presented. Taken together, it appears that seasonal fluctuations in immune parameters, mediated by melatonin, could have profound effects on the etiology and progression of diseases in humans and nonhuman animals. An adaptive functional perspective is critical to gain insights into the interaction among melatonin, immune function, and disease processes.
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PMID:The influence of season, photoperiod, and pineal melatonin on immune function. 878 46

Winter is energetically demanding. Physiological and behavioral adaptations have evolved among nontropical animals to cope with winter because thermoregulatory demands increase when food availability decreases. Seasonal breeding is central within the suite of winter adaptations among small animals. Presumably, reproductive inhibition during winter conserves energy at a time when the adds of producing viable young are low. In addition to the well-studied seasonal cycles of mating and birth, there are also significant seasonal cycles of illness and death among many populations of mammals and birds in the field. Challenging winter conditions, such as low ambient temperatures and decreased food availability, can directly induce death via hypothermia, starvation or shock. In some cases, survival in demanding winter conditions puts individuals under great physiological stress, defined here as an adaptive process that results in elevated blood levels of glucocorticoids. The stress of coping with energetically demanding conditions can also indirectly cause illness and death by compromising immune function. Presumably, the increased blood concentrations of adrenocortical steroids in response to winter stressors compromise immune function and accelerate catabolic mechanisms in the field, although the physiological effects of elevated glucocorticoids induced by artificial stressors have been investigated primarily in the laboratory. However, recurrent environmental stressors could reduce survival if they evoke persistent glucocorticoid secretion. The working hypothesis of this article is that mechanisms have evolved in some animals to combat seasonal stress-induced immunocompromise as a temporal adaptation to promote survival. Furthermore, we hypothesize that mechanisms have evolved that allow individuals to anticipate periods of immunologically challenging conditions, and to cope with these seasonal health-threatening conditions. The primary environmental cue that permits physiological anticipation of season is the daily photoperiod; however, other environmental factors may interact with photoperiod to affect immune function and disease processes. The evidence for seasonal fluctuations in lymphatic organ size, structure, immune function, and disease processes, and their possible interactions with recurrent environmental stressors, is reviewed. Seasonal peaks of lymphatic organ size and structure generally occur in late autumn or early winter and seasonal minima are observed prior to the onset of breeding. Although many of the field data suggest that immune function and disease processes are also enhanced during the winter, the opposite seasonal pattern is also observed in some studies. We propose that compromised immune function may be observed in some populations during particularly harsh winters when stressors override the enhancement of immune function evoked by short day lengths. Because so many factors covary in field studies, assessment of our proposal that photoperiod mediates seasonal changes in immune function requires laboratory studies in which only photoperiod is varied. A review of the effects of photoperiod on immune function in laboratory studies reveals that exposure to short day lengths enhances immune function in every species examined. Short day exposure in small mammals causes reproductive inhibition and concomitant reduction in plasma levels of prolactin and steroid hormones, as well as alterations in the temporal pattern of pineal melatonin secretion. These hormones affect immune function, and influence the development of opportunistic diseases, including cancer: however, it appears that either prolactin or melatonin secretion is responsible for mediating the effects of photoperiod on immune function. Taken together, day length appears to affect immune function in many species, including animals that typically do not exhibit reproductive responsiveness to day length.
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PMID:Seasonal changes in immune function. 898 73

Winter is energetically demanding and stressful; thermoregulatory demands increase when food availability usually decreases. Physiological and behavioral adaptations, including termination of breeding, have evolved among nontropical animals to cope with the energy shortages during winter. Presumably, selection for the mechanisms that permit physiological and behavioral anticipation of seasonal ambient changes have led to current seasonal breeding patterns for many populations. In addition to the well-studied seasonal cycles of mating and birth, there are also significant seasonal cycles of illness and death among field populations of mammals and birds. Energetically challenging winter conditions can directly induce death via hypothermia, starvation, or shock; surviving these demanding conditions likely puts individuals under great physiological stress. The stress of coping with energetically demanding conditions may increase adrenocortical steroid levels that could indirectly cause illness and death by compromising immune function. Individuals would enjoy a survival advantage if seasonally recurring stressors could be anticipated and countered by bolstering immune function. The primary environmental cue that permits physiological anticipation of season is daily photoperiod, a cue that is mediated by melatonin. However, other environmental factors may interact with photoperiod to affect immune function and disease processes. Immune function is compromised during the winter in field studies of birds and mammals. However, laboratory studies of seasonal changes in mammalian immunity consistently report that immune function is enhanced in short day lengths. To resolve this apparent discrepancy, we hypothesize that winter stressors present in field studies counteract short-day enhancement of immune function. Prolonged melatonin treatment mimics short days, and also enhances rodent immune function. Reproductive responsiveness to melatonin appears to affect immune function. In sum, melatonin may be part of an integrative system to coordinate reproductive, immunologic, and other physiological processes to cope successfully with energetic stressors during winter.
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PMID:Role of melatonin in mediating seasonal energetic and immunologic adaptations. 937 Feb 7

Chronic cold exposure stimulates sympathetically driven thermogenesis in brown adipose tissue (BAT), resulting in fat mobilization, weight loss, and compensatory hyperphagia. Hypothalamic neuropeptide Y (NPY) neurons are implicated in stimulating food intake in starvation, but may also suppress sympathetic outflow to BAT. This study investigated whether the NPY neurons drive hyperphagia in rats that have lost weight through cold exposure. Rats exposed to 4 degrees C for 21 days weighed 14% less than controls maintained at 22 degrees C (P < 0.001). Food intake increased after 3 days and remained 10% higher thereafter (P < 0.001). Increase BAT activity was confirmed by 64, 96, and 335% increases in uncoupling protein-1 mRNA at 2, 8, and 21 days. Plasma leptin decreased during prolonged cold exposure. Cold-exposed rats showed no significant changes in NPY concentrations in any hypothalamic regions or in hypothalamic NPY mRNA at any time. We conclude that the NPY neurons are not activated during cold exposure. This is in contrast with starvation-induced hyperphagia, but is biologically appropriate since enhanced NPY release would inhibit thermogenesis causing potentially lethal hypothermia. Other neuronal pathways must therefore mediate hyperphagia in chronic cold exposure.
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PMID:Hyperphagia in cold-exposed rats is accompanied by decreased plasma leptin but unchanged hypothalamic NPY. 945 99

To clarify the pathogenesis of the widely known but obscure syndrome of sudden death with hepatic fatty metamorphosis observed in alcohol abusers, we have scrutinized both the clinical and pathological data of 11 subjects who died under such circumstances between 1987 and 1993. Death followed several days of uninterrupted drinking often with little dietary intake. The notable clinical features on arrival at the emergency room were disturbance of consciousness (11/11), hypotension (4/6), hypothermia (3/5), hypoglycaemia (8/11), metabolic acidosis (6/6), renal dysfunction (11/11), and hyperammonaemia (5/5). The common hepatic pathology was the extensive appearance of numerous microvesicular fatty droplets in the hepatocytes together with varying degrees of macrovesicular fatty change; four subjects had an underlying cirrhosis. Death undoubtedly results from a variety of metabolic disturbances triggered by the combination of massive ethanol intake and starvation. The appearance of extensive microvesicular fatty change superimposed on macrovesicular fatty change was considered to be an associated phenomenon.
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PMID:Alcohol-related sudden death with hepatic fatty metamorphosis: a comprehensive clinicopathological inquiry into its pathogenesis. 946 29


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