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PubMed1982

Vasopressin and the regulation of evaporative water loss and body temperature in the cat.

The role of vasopressin as a possible mediator of the inhibition of evaporative water loss (EWL) in dehydrated, heat-stressed cats has been examined by intravenous (i.v.) and intracerebroventricular (i.c.v.) injections of arginine vasopressin (AVP). In normally hydrated cats exposed to an ambient temperature (Ta) of 38 degrees C, neither EWL nor body temperature (Tb), measured in the hypothalamus, was significantly altered by i.v. AVP infusion. Measurements of plasma osmolality (pOsm), pAVP and cerebrospinal fluid AVP (csfAVP) were made in normally hydrated cats at Tas of 25 and 38 degrees C and after dehydration for 1-4 days at these temperatures. The relationship between pOsm and pAVP can be described equally well by either a linear model or a log-linear model (r = 0.81 for both models). The pOsm-csfAVP relationship is best described by a log-linear model (r = 0.80). A possible role for intracranially released AVP in body temperature regulation and control of EWL was examined by injecting various doses of AVP into the lateral ventricles of normally hydrated cats. No effect of AVP injection on Tb was observed at either a Ta of 23 degrees C or 38 degrees C. EWL was also unaffected by i.c.v. AVP administration at a Ta of 38 degrees C. To confirm further that intracranial AVP is not responsible for elevation of Tb and reduction of EWL during dehydration and heat-stress, specific antiserum to AVP was injected into the ventricles of dehydrated animals at a Ta of 38 degrees C. No significant effect on either Tb or EWL was measured subsequent to antiserum infusion. These negative findings indicate that AVP does not suppress EWL by either a peripheral or a central action and is therefore not responsible for lowered EWL and elevated Tb seen in dehydrated heat-stressed cats.

Animals↗
PubMed2003

Regulation of body temperature and neuroprotection by endogenous interleukin-6 in cerebral ischemia.

Although the function of fever is still unclear, it is now beyond doubt that body temperature influences the outcome of brain damage. An elevated body temperature is often found in stroke patients and denotes a bad prognosis. However, the pathophysiologic basis and treatment options of elevated body temperature after stroke are still unknown. Cerebral ischemia rapidly induced neuronal interleukin-6 (IL-6) expression in mice. In IL-6-deficient mice, body temperature was markedly decreased after middle cerebral artery occlusion (MCAO), but infarct size was comparable to that in control mice. If body temperature was controlled by external warming after MCAO, IL-6-deficient mice had a reduced survival, worse neurologic status, and larger infarcts than control animals. In cell culture, IL-6 exerted an antiapoptotic and neuroprotective effect. These data suggest that IL-6 is a key regulator of body temperature and an endogenous neuroprotectant in cerebral ischemia. Neuroprotective properties apparently compensate for its pyretic action after MCAO and enhance the safety of this endogenous pyrogen.

Animals↗
PubMed2006

Hepatocyte NF-kappaB activation is hepatoprotective during ischemia-reperfusion injury and is augmented by ischemic hypothermia.

The present study examined the role of hepatocyte NF-kappaB activation during ischemia-reperfusion injury. Second, we evaluated the effects of ischemic hypothermia on NF-kappaB activation and liver injury. C57BL/6 mice underwent 90 min of partial hepatic ischemia and up to 8 h of reperfusion. Body temperature was regulated during the ischemic period between 35 and 37 degrees C, 33 and 35 degrees C, 29 and 33 degrees C or unregulated, where temperature fell to <29 degrees C. Liver injury, as measured by serum alanine aminotransferase as well as liver histopathology, was inversely proportional to regulated body temperature, with the unregulated group (<29 degrees C) being highly protected and the normothermic group (35-37 degrees C) displaying the greatest injury. Inflammation, as measured by production of TNF-alpha and liver recruitment of neutrophils, was greatest in the normothermic groups and lowest in the ischemic hypothermia groups. Interestingly, hepatocyte NF-kappaB activation was highest in the hypothermic group and least in the normothermic group. Paradoxically, degradation of IkappaB proteins, IkappaB-alpha and IkappaB-beta, was greatest in the normothermic group, suggesting an alternate NF-kappaB regulatory mechanism during ischemia-reperfusion injury. Subsequently, we found that NF-kappaB p65 protein was increasingly degraded in normothermic versus hypothermic groups, and this degradation was specific for hepatocytes and was associated with decreased expression of the peptidyl-prolyl isomerase Pin1. The data suggest that NF-kappaB activation in hepatocytes is a protective response during ischemia-reperfusion and can be augmented by ischemic hypothermia. Furthermore, it appears that Pin1 promotes NF-kappaB p65 protein stability such that decreased expression of Pin1 during ischemia-reperfusion results in p65 degradation, reduced nuclear translocation of NF-kappaB, and enhanced hepatocellular injury.

Alanine Transaminase↗
PubMed1977

Thermoregulatory responses to altering hypothalamic temperature in the harbor seal.

The rostral brainstem of the harbor seal Phoca vitulina was cooled and heated 33-41 degrees C while oxygen consumption and rectal, hypothalamic, flipper and dorsal skin temperatures were measured. These experiments were made on restrained seals at ambient temperatures -15 to 30 degrees C. Cooling the preoptic and hypothalamic (POH) tissue increased oxygen consumption in a way that could be approximated by a linear regression line with slope and threshold temperature at which the metabolic rate was minimal. The slope of the regression line was a function of ambient temperature and rectal temperature. At each ambient temperature, the slope was significantly higher for lower rectal temperature. At all rectal temperatures, the slope was significantly higher for lower ambient temperature. The threshold hypothalamic temperatures did not very consistently or significantly with either rectal temperature or ambient temperature. These results on the harbor seal are explicable by suggesting that the thermal-sensitive and reference neurons in the POH which regulate body temperature are inhibited equally by extrahypothalamic cold transducing neural elements.

Animals↗
PubMed2002

Neurovestibular modulation of circadian and homeostatic regulation: vestibulohypothalamic connection?

Chronic exposure to increased force environments (+G) has pronounced effects on the circadian and homeostatic regulation of body temperature (T(b)), ambulatory activity (Act), heart rate, feeding, and adiposity. By using the Brn 3.1 knockout mouse, which lacks vestibular hair cells, we recently described a major role of the vestibular system in mediating some of these adaptive responses. The present study used the C57BL6JEi-het mouse strain (het), which lacks macular otoconia, to elucidate the contribution of specific vestibular receptors. In this study, eight het and eight WT mice were exposed to 2G for 8 weeks by means of chronic centrifugation. In addition, eight het and eight WT mice were maintained as 1G controls in similar conditions. Upon 2G exposure, the WT exhibited a decrease in T(b) and an attenuated T(b) circadian rhythm. Act means and rhythms also were attenuated. Body mass and food intake were significantly lower than the 1G controls. After 8 weeks, percent body fat was significantly lower in the WT mice (P < 0.0001). In contrast, the het mice did not exhibit a decrease in mean T(b) and only a slight decrease in T(b) circadian amplitude. het Act levels were attenuated similarly to the WT mice. Body mass and food intake were only slightly attenuated in the het mice, and percent body fat, after 8 weeks, was not different in the 2G het group. These results link the vestibular macular receptors with specific alterations in homeostatic and circadian regulation.

Acceleration↗
PubMed1994

Effect of modafinil on heat production and regulation of body temperatures in cold-exposed humans.

Military personnel often undergo sustained operations that affect vigilance and alertness. Pharmacological agents may be used to enhance vigilance. Most such agents also have thermogenic properties. Whether a new promising stimulant, modafinil (Lyons and French, Aviat. Space Environ. Med. 1991; 62:432-435), has a beneficial effect on cold tolerance in the military context, is not known. The goal of this study was, therefore, to evaluate the effect of this new drug on thermal balance and the regulation of body temperatures in neutral conditions and when challenged by a cold exposure. Nine subjects underwent three trials each: two in the cold (3 h at rest, 10 degrees C) 0.5 h after the ingestion of either placebo or modafinil (200 mg), and one in thermal neutrality with modafinil (same conditions except Tdb = 29.3 degrees C). As expected, cold produced a drop in Tre and Tsk and an increase in Vo2. Although non-significant, there was a tendency for a slightly greater drop in Tre with modafinil (0.65 degrees C vs. 0.57 degrees C with placebo). A similar tendency was found for the heat debt (S) which was greater with modafinil than with placebo (16.1 +/- 0.7 vs. 14.7 +/- 0.6 kJ.kg-1, respectively, +9.5%, p = 0.11). This tendency appears to be the combined result of a slightly lower mean heat production during the test and a slightly greater mean dry heat loss. When tested at thermal neutrality, the drug had no effect on any thermal or metabolic parameters. The results demonstrate that the ingestion of a single dose of modafinil has no significant acute effect on thermal balance in neutral conditions and on thermoregulation in normal subjects exposed to cold. However, a tendency for slightly greater cooling was noted with modafinil. It is not known whether the use of modafinil in conjunction with sleep deprivation (a likely scenario) could magnify this effect.

Adult↗
PubMed2003

Changes in selected ambient temperatures following physical training in rats.

To clarify the mechanism of body temperature (T(b)) rise following voluntary wheel-run training in rats, we investigated the behavioral thermoregulation in female rats by means of a thermal gradient system. We performed thermal gradient tests before training, 4 weeks after training started, and 2 weeks after it stopped. We also examined the effects on the selected ambient temperature and T(b) with quantitative training activity. Nine female rats ran voluntarily in a wheel in the range of 6,545 from 1,665 revolutions/night. The higher the wheel-running activity, the higher the T(b) level rose at rest during the daytime after 4 weeks of training. The higher-activity rats selected a higher ambient temperature after the training than before, and the T(b) was maintained at a high level under this environment. Our results suggest that the rise in T(b) level during rest following the wheel-run training is a regulated body temperature change.

Animals↗
PubMed1982

Facial thermal input in the caudal trigeminal nucleus of rats reared at 30 degrees C.

1. Rats reared from birth in air at 30 degrees C showed a decreased ability to maintain colonic temperature when exposed to 10 degrees C as compared with rats reared at 20 degrees C. This difference was not due to physical factors affecting heat loss, such as surface area or fur thickness. 2. In anaesthetized rats extracellular recordings were made in trigeminal nucleus caudalis from higher order neurones with input from facial cold and warm receptors. A systematic search on a grid pattern showed there was no difference between heat-reared and control rats in facial receptive fields or in the abundance, extent and somatotopic distribution of thermal neurones in the nucleus. In both groups almost all the neurones were excited only by facial cooling. 3. When single cold neurones were tested quantitatively by the application of controlled temperature changes to their receptive fields on the face there was no difference in the static temperature/discharge rate relationship between the two groups of rats. 4. The results suggest that the observed difference in ability to regulate body temperature is not attributable to differences in skin-temperature reception at the level of the trigeminal nucleus.

Animals↗
PubMed1991

[A study on thermal regulation disturbance in severely handicapped patients].

Forty-five severely handicapped patients were investigated on body temperature regulation. Poor regulation cases had CT scans showing severe third and lateral ventricle dilatation. Furthermore, in almost all poor regulation cases of perinatal and postnatal onset, CT scans showed extensive low density areas involving the frontal lobe. Electrophysiological studies (sSEP, ABR and blink reflex) could not show definite differences between poor regulation cases and good regulation cases. These findings suggest that hypothalamus, medial forebrain bundle and frontal lobe play important roles in body temperature regulation. On the other hand, perinatal or postnatal onset cases frequently had small body surface areas and low serum creatinine.

Adolescent↗
PubMed1980

Thermoregulation in Telazol (CI-744)-anesthetized rhesus monkey (Macaca mulatta).

Seven Telazol (CI-744)-[Telazol is an experimental drug (Parke, Davis) composed of two ingredients in equal amounts by weight: tiletamine HCl, designated chemically as 2-(ethylamino)-2-(2-thienyl)cyclohexanone-HCl, and zolazepam HCl, designated as 4-(o-fluorophenyl)-6,8-dihydro-1,3,8-trimethylpyrazolo-3,4-e 1,4 diazepin-7(IH)-one monohydrochloride] anesthetized rhesus monkeys (Macaca mulatta) were exposed to ambient temperatures (Ta) of 15, 23, 29, 35, and 38 degrees C to evaluate the effect of this dissociative anesthetic agent on thermoregulation. Thermal equilibrium in both anesthetized and control animals at Ta 15 degrees C was through peripheral vasoconstriction and metabolic heat production (M); shivering increased M in the anesthetized group to 1.7 times the resting M of 41.4 W x m-2. Both groups at Ta 38 degrees C regulated body temperature by vasodilation and increased skin evaporative heat loss (Esk) due to sweating. Anesthetized animals increased Esk from 6.4 W x m-2 at Ta 29 degrees C to 32.5 W x m-2 at Ta 38 degrees C. Panting was not observed in either group. Effective tissue thermal conductance was lowest at Ta 15 and 23 degrees C (6.9 and 7.6 W x m2 x degrees C-1, respectively), and increased with Ta's above 23 degrees C (45.0 W x m-2 at Ta 38 degrees C). These results indicate that Telazol-anesthetized monkeys maintain thermal balance at ambient temperatures from 15 to 38 degrees C, and that Telazol induces little or no impairment of thermoregulation in rhesus monkeys.

Anesthesia↗
PubMed1995

Thermosensitive phenotype of transgenic mice overproducing human glutathione peroxidases.

Exposure of humans and other mammals to hyperthermic conditions elicits many physiological responses to stress in various tissues leading to profound injuries, which eventually result in death. It has been suggested that hyperthermia may increase oxidative stress in tissues to form reactive oxygen species harmful to cellular functions. By using transgenic mice with human antioxidant genes, we demonstrate that the overproduction of glutathione peroxidase (GP, both extracellular and intracellular) leads to a thermosensitive phenotype, whereas the overproduction of Cu,Zn-superoxide dismutase has no effect on the thermosensitivity of transgenic mice. Induction of HSP70 in brain, lung, and muscle in GP transgenic mice at elevated temperature was significantly inhibited in comparison to normal animals. Measurement of peroxide production in regions normally displaying induction of HSP70 under hyperthermia revealed high levels of peroxides in normal mice and low levels in GP transgenic mice. There was also a significant difference between normal and intracellular GP transgenic mice in level of prostaglandin E2 in hypothalamus and cerebellum. These data suggest direct participation of peroxides in induction of cytoprotective proteins (HSP70) and cellular mechanisms regulating body temperature. GP transgenic mice provide a model for studying thermoregulation and processes involving actions of hydroxy and lipid peroxides in mammals.

Animals↗
PubMed1981

Thermal balance in ketamine-anesthetized rhesus monkey Macaca mulatta.

A partitional calorimetry study compared thermoregulatory responses of unanesthetized adult rhesus monkeys (4 female, 1 male) to those anesthetized with ketamine HCl and exposed to ambient temperature (Ta) of 18, 29, 38 degrees C. Steady-state metabolic heat production (M), mean skin temperature (Tsk), rectal temperature (Tre), respiratory evaporative heat loss (Eres), and total evaporative heat loss (Etot) were measured at each Ta. Average Tre of anesthetized animals was reduced by approximately 1 degree C at Ta 18 degrees C, but thermal balance in anesthetized and control animals was maintained by reflexly decreased tissue conductance and shivering. For anesthetized animals, the average M increased 1.8 times over the lowest value of 40.13 W/m2 at Ta 29 degrees C, compared to a 1.5-fold increase for controls. Responses for both groups were not different at Ta 29 degrees C, both groups regulated body temperatures by vasodilation and increased sweating, but with ketamine sweating was reduced (35%). Effective tissue thermal conductance (K) was lowest at Ta 18 (10.8 W/m2 . degrees C) and increased to 39.4 W/m2 . degrees C at Ta 38 degrees C. No significant difference in K was found between ketamine and control groups at other Ta's.

Animals↗
PubMed1983

Prenatal phenobarbital treatment and temperature-controlling dopamine receptors.

Pregnant mice were fed a phenobarbital-containing diet on days nine through 18 of pregnancy. Following parturition, the offspring of such animals were allowed to reach adulthood and then were tested for their response to an acute injection of apomorphine. Male offspring were less sensitive, while female offspring were more sensitive than matched controls to apomorphine-induced hypothermia. The witnessed differences in apomorphine-induced hypothermia could not be attributed to differences in brain apomorphine levels, alterations in the thermoregulation following non-drug challenges to the mouse's thermoregulatory ability, or changes in alpha-adrenergic receptor function. Our results suggest that prenatal phenobarbital administration produces changes in the function of dopamine receptors which regulate body temperature, and that the prenatally-induced changes last well into adulthood.

Animals↗
PubMed1984

[Diabetic neuropathies. IV. Autonomous neuropathy. Peripheral sympathetic innervation and the cardiovascular system].

The clinical conditions due to damage to the peripheral sympathetic nervous system during diabetic neuropathy mainly involve alterations to subcutaneous vasomotility , temperature body regulation and exudation, which may take form of hyper or hypoactivity. Gustatory exudation and local anhydrosis are described in detail as well as the connection with aggravating factors like long duration, poor balance and early onset of diabetes mellitus . Change in the relevant cardiovascular reflexes, commonly used in diagnosing diabetic neuropathy, are also analysed with a discussion of their physiopathological background and clinical significance. Finally the painless infarct, sudden death and abnormal response to hypoglycaemia, that are the common features of diabetic neuropathy, are also described.

Body Temperature Regulation↗
PubMed1984

Thermoregulatory responses to exercise in dehydrated dogs.

Measurements of rectal temperature (Tre), water lost by evaporation (Eresp) and drooling, cardiac output (CO), and common carotid blood flow (CCBF) were made in dogs (mean hydrated wt 31.0 +/- 1.5 kg) running for 1 h on a level treadmill at 7.5 km/h at an ambient temperature of 25 degrees C. Each animal was studied when it was hydrated ad libitum and when it had been dehydrated by removal of drinking water until 9-10% of the initial body weight had been lost. Dehydrated exercising animals had significantly higher Tre and lower rates of Eresp, CO, and CCBF. Tre and Eresp were measured in seven animals. Average Tre during running was 39.11 +/- 0.10 degrees C in hydrated and 39.80 +/- 0.25 degrees C in dehydrated animals (P less than 0.01). Average Eresp during running was 3.9 +/- 0.3 g/min in hydrated animals and 2.3 +/- 0.3 g/min in dehydrated animals (P less than 0.01). Average CO during exercise, measured in five animals, was 11.1 +/- 0.7 1/min in the hydrated state and 8.6 +/- 0.5 1/min in the dehydrated state (P less than 0.01). Unilateral CCBF during exercise, measured in four animals, was 602 +/- 40 ml/min in the hydrated state and 418 +/- 22 ml/min in the dehydrated state (P less than 0.01). Water lost by drooling in seven exercising animals was 41.5 +/- 11 g/h when they were hydrated and 0.6 +/- 0.4 g/h when they were dehydrated. It is concluded that dehydrated dogs doing mild exercise can save water by reducing Eresp and regulating body temperature above hydrated levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Microinjection of neurotensin into the ventral tegmental area produces hypothermia: evaluation of dopaminergic mediation.

Neurotensin-producing perikarya and fibers have been identified in the ventral tegmental area of the rat, and recent microinjection studies indicate that neurotensin may function in the ventral tegmental area to regulate body temperature. In this study, the hypothermic response produced by intraventral tegmental injection of neurotensin was shown to be dose-dependent, with a threshold dose between 0.25 and 0.75 micrograms. When fluphenazine, a dopamine receptor antagonist, was microinjected into various forebrain nuclei simultaneous with neurotensin infusion into the ventral tegmental area, it was found to block neurotensin hypothermia. In contrast, injection with fluphenazine into the nucleus accumbens, lateral septum or preoptic area did not alter the hypothermic response. Furthermore, injection with atropine, phentolamine or diphenhydramine into the diagonal band of Broca did not block neurotensin hypothermia. Neurotensin was also injected directly into the preoptic region and shown to produce hypothermia. However, concurrent infusion of fluphenazine with neurotensin into the preoptic region did not attenuate neurotensin hypothermia. These data are consistent with the postulate that neurotensin acts in the ventral tegmental area to enhance dopamine release in the diagonal band of Broca, thereby producing hypothermia. However, neurotensin-induced hypothermia occurring after injection into the preoptic area does not appear to involve dopamine systems.

Animals↗