Thermoregulatory responses to acute body heating in rats acclimated to continuous heat exposure

Thermoregulatory responses to an acute heat load with intraperitoneal heating (IH) or indirect external warming (EW) by increasing ambient temperature (Ta) were investigated with direct and indirect calorimetry in rats acclimated to environments of 24.0 degrees C (Cn), 29.4 degrees C (H1), and 32.8 degrees C (H2) for greater than 15 days. The rats were placed in a direct calorimeter where the air temperature was maintained at 24 degrees C for the initial 3 h. IH was then made for 30 min through an electric heater implanted chronically (6.5 W.kg-1) in the peritoneal cavity, and EW was performed by raising the jacket water temperature surrounding the calorimeter from 24 to 39 degrees C (0.19 degrees C.min-1). Hypothalamic (Thy) and colonic temperature immediately before the start of the heat load tended to be higher as the acclimation temperature increased. During IH, the threshold Thy for the tail skin vasodilation (Tth) was significantly higher in H2 than in Cn rats. During EW, however, there was no difference in Tth between the groups. Metabolic heat production (M) was slightly suppressed during IH and significantly depressed only in H2 rats. During EW, M was suppressed in all the groups. The magnitude and duration of suppression were greater in H2 rats than in the other two groups. The responses in nonevaporative heat loss and thermal conductance (C) to the rise in Thy did not differ among the three groups during IH. According to the rise in Thy, however, there was a greater C increase in H2 than in Cn and H1 rats during EW.(ABSTRACT TRUNCATED AT 250 WORDS)     

Central angiotensin receptor blockade impairs thermolytic and dipsogenic responses to heat exposure in rats

The effect of central angiotensin AT(1) receptor blockade on thermoregulation and water intake after heat exposure was investigated. Rats were placed in a chamber heated to 39 +/- 1 degrees C for 60 min and then returned to their normal cage (at 22 degrees C), and water intake was measured for 120 min. Artificial cerebrospinal fluid (5 microl) was injected intracerebroventricularly 60 min before heat exposure in five control rats. Colonic temperature increased from 37.22 +/- 0.21 to 40.68 +/- 0.31 degrees C after 60 min. In six rats injected intracerebroventricularly with 10 microg of the AT(1) antagonist losartan, colonic temperature increased from 37.41 +/- 0.27 to 41.72 +/- 0.28 degrees C after 60 min. This increase was significantly greater than controls (P < 0.03). Losartan-treated rats drank 1.1 +/- 0.4 ml of water compared with 5.9 +/- 0.77 ml (P < 0.002) drank by control animals, despite a similar body weight loss in the two groups. Central losartan did not inhibit the drinking response to intracerebroventricular carbachol in heated rats, suggesting that losartan treatment did not nonspecifically depress behavior. We conclude that central angiotensinergic mechanisms have a role in both thermoregulatory cooling in response to heat exposure and also the ensuing water intake.     

Circadian variations in psychophysiological responses to heat exposure and exercise

Ten healthy men were tested at 0600, 1200, 1800 and 2400 hours on different days at rest in a laboratory at room temperature followed by 1 h of heat exposure in a climatic chamber at 42 degrees C, 60% rh (50 min rest and 10 min exercise on a cycle ergometer at 50% VO2max). Heart rate, blood pressure, rectal temperature Tre, metabolic rate, number connection test, visual and auditory reaction time, flicker test and catecholamine excretion were measured. Heat exposure and exercise caused lower heart rate acceleration at 2400 hours than at 0600 and 1200 hours, the smallest increase of Tre at 1800 hours, and an increase in metabolic rate greater at 1200 than at 1800 hours. In the afternoon, when, according to the circadian rhythm, the body temperature is highest, the additional heat load produced the smallest physiological effects. Performance efficiency, after heat exposure combined with physical exercise, improved slightly, but diurnal variations did not show significant circadian rhythm.     

Testosterone modifies response to chronic heat exposure in rats

Eight weeks of heat exposure (34±0.5°C) in sham-orchiectomized rats leads to an increase of body temperature, slowing of body growth rate, and decrease of serum corticosterone level, as compared with animals maintained at 21±2°C. Orchiectomy decreases body temperature, slows growth rate, and increases plasma corticosterone concentration both in control and heat exposed animals. Testosterone administration reverts these parameters to initial values. We conclude that testosterone plays a role in the regulation of heat balance in male rats.     

Chronic prenatal exposure to cocaine alters cerebrovascular responses in newborn pigs

Maternal cocaine abuse may increase the incidence of perinatal asphyxia. In nonexposed asphyxiated neonates, decreased cerebrospinal fluid (CSF) cAMP concentrations are associated with poor neurological outcome. On the other hand, cocaine increases central nervous system (CNS) cAMP. Therefore, we hypothesized that in utero cocaine exposure may increase brain cAMP and thereby preserve cerebrovascular responses to cAMP-dependent stimuli following asphyxia. Pregnant pigs received either cocaine (1 mg/kg, i.v.) twice weekly during the last trimester or normal saline vehicle (sham-control) and were allowed to deliver vaginally at term. Cranial windows were implanted in the newborn pigs within the first week of life and used to collect CSF for cAMP determinations and to assess changes in pial arteriolar diameters (PAD). In the first part of the study, pial arteriolar responses to different vasodilator and vasoconstrictor stimuli were evaluated in piglets prior to asphyxia (n = 20). In newborn pigs exposed to cocaine, cerebrovascular responses to hypercapnia and norepinephrine were significantly exaggerated compared to controls. Then, piglets were randomly selected for the second part of the study that involved prolonged asphyxia (n = 12). In cocaine-exposed but not sham-control piglets, CSF cAMP increased markedly during asphyxia. In the sham piglets, but not the cocaine-exposed piglets, CSF cAMP fell progressively below the baseline during recovery. Cerebrovascular reactivity to cAMP-dependent stimuli (hypercapnia and isoproterenol) was preserved during recovery from asphyxia in the cocaine-exposed piglets but significantly attenuated in the sham controls. We conclude that piglets with chronic prenatal exposure to cocaine show exaggerated cerebrovascular responses to vasogenic stimuli and preserved cAMP-dependent cerebral vasoreactivity following asphyxia.     

A conspecific attenuates prolactin responses to open-field exposure in rats

Acute exposure to a novel environment, such as an open field, generally results in a prolactin surge, while several days of exposure to the open field is often characterized by a decline in prolactin. As exposure to the open field is a psychological stressor, altering the animal's interpretation of the event should alter prolactin levels. In the present study, juvenile male and female rats were habituated to the open field for 1 or 5 days prior to testing in the chamber alone or with a same-sex conspecific. Levels of prolactin were measured across all rats, and play (pins) was recorded for animals tested with a conspecific. Five days of habituation to the chamber resulted in lower levels of prolactin and more play than 1 day of habituation. Across both conditions of habituation, testing with a conspecific caused lower levels of prolactin than testing alone. In addition, play and prolactin were negatively correlated. The presence of a conspecific in a stressful situation may have reduced stress by altering the animal's negative interpretation of the open field. Further, as the intensity of the social interaction increased (more play), prolactin levels decreased.     

Antioxidative and metabolic responses to extended cold exposure in rats

In this work, we investigated whether extended cold exposure increases oxidative damage and susceptibility to oxidants of rat liver, heart, kidney and lung which are metabolically active tissues. Moreover in this study the effect of cold stress on some of the lipid metabolic mediators were studied in rat experimental model. Male albino Sprague-Dawley rats were randomly divided into two groups: The control group (n=12) and the cold-stress group (n=12). Tissue superoxide dismutase (SOD), catalase (CAT), glutathion S-transferase (GST) and glutathion reductase (GR) activities and glutathion (GSH) were measured using standard protocols. The biochemical analyses for total lipid, cholesterol, trigliceride, HDL, VLDL and LDL were done on autoanalyzer. In cold-stress groups SOD activity was decreased in the lung whereas it increased in the heart and kidney. CAT activity was significantly decreased (except liver) in all the tissues in treated rats. GST activity of cold-induced rats increased in liver and heart while decreased in the lung. GR activity was significantly decreased (except in liver) in all the tissues in cold-stressed rats. GSH level was significantly increased in the heart but decreased in the lung of animals exposed to cold when compared to controls. It was found that among the groups trigliceride, total lipid, HDL and VLDL parameters varied significantly but cholesterol and LDL had no significant variance. In this study, we found that exposure of extended (48 h) cold (8 degrees C) caused changes both in the antioxidant defense system (as tissue and enzyme specific) and serum lipoprotein profiles in rats.     

Heat loss responses in rats acclimated to heat loaded intermittently

The present study examined the heat loss response of heat-acclimated rats to direct body heating with an intraperitoneal heater or to indirect warming by elevating the ambient temperature (Ta). The heat acclimation of the rats was attained through exposure to Ta of 33 or 36 degrees C for 5 h daily during 15 consecutive days. Control rats were kept at Ta of 24 degrees C for the same acclimation period. Heat acclimation lowered the body core temperature at Ta of 24 degrees C, and the core temperature level was lowered as acclimation temperature increased. When heat was applied by direct body heating, the threshold hypothalamic temperature (Thy) for the tail skin vasodilation was also lower in heat-acclimated rats than in the control rats. However, the amount of increase in Thy from the resting level to the threshold was the same in all three groups. When heat was applied by indirect warming, threshold Thy was slightly higher in heat-acclimated than in control rats. The amount of increase in Thy from the resting level to the threshold was significantly greater in heat-acclimated rats. In addition, Ta and the skin temperature at the onset of skin vasodilation were significantly higher in heat-acclimated rats. The results indicate that heat-acclimated rats were less sensitive to the increase in skin temperature in terms of threshold Thy. The gain constant of nonevaporative heat loss response was assessed by plotting total thermal conductance against Thy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic fetal exposure to Ureaplasma parvum suppresses innate immune responses in sheep

The chorioamnionitis associated with preterm delivery is often polymicrobial with ureaplasma being the most common isolate. To evaluate interactions between the different proinflammatory mediators, we hypothesized that ureaplasma exposure would increase fetal responsiveness to LPS. Fetal sheep were given intra-amniotic (IA) injections of media (control) or Ureaplasma parvum serovar 3 either 7 or 70 d before preterm delivery. Another group received an IA injection of Escherichia coli LPS 2 d prior to delivery. To test for interactions, IA U. parvum-exposed animals were challenged with IA LPS and delivered 2 d later. All animals were delivered at 124 ± 1-d gestation (term = 150 d). Compared with the 2-d LPS exposure group, the U. parvum 70 d + LPS group had 1) decreased lung pro- and anti-inflammatory cytokine expression and 2) fewer CD3(+) T lymphocytes, CCL2(+), myeloperoxidase(+), and PU.1(+) cells in the lung. Interestingly, exposure to U. parvum for 7 d did not change responses to a subsequent IA LPS challenge, and exposure to IA U. parvum alone induced mild lung inflammation. Exposure to U. parvum increased pulmonary TGF-β1 expression but did not change mRNA expression of either the receptor TLR4 or some of the downstream mediators in the lung. Monocytes from fetal blood and lung isolated from U. parvum 70 d + LPS but not U. parvum 7 d + LPS animals had decreased in vitro responsiveness to LPS. These results are consistent with the novel finding of downregulation of LPS responses by chronic but not acute fetal exposures to U. parvum. The findings increase our understanding of how chorioamnionitis-exposed preterm infants may respond to lung injury and postnatal nosocomial infections.     

Chronic exposure to corticosterone enhances the neuroinflammatory and neurotoxic responses to methamphetamine

J. Neurochem. (2012) 122, 995-1009. ABSTRACT: Up-regulation of proinflammatory cytokines and chemokines in brain ("neuroinflammation") accompanies neurological disease and neurotoxicity. Previously, we documented a striatal neuroinflammatory response to acute administration of a neurotoxic dose of methamphetamine (METH), i.e. one associated with evidence of dopaminergic terminal damage and activation of microglia and astroglia. When we used minocycline to suppress METH-induced neuroinflammation, indices of dopaminergic neurotoxicity were not affected, but suppression of neuroinflammation was incomplete. Here, we administered the classic anti-inflammatory glucocorticoid, corticosterone (CORT), in an attempt to completely suppress METH-related neuroinflammation. METH alone caused large increases in striatal proinflammatory cytokine/chemokine mRNA and subsequent astrocytic hypertrophy, microglial activation, and dopaminergic nerve terminal damage. Pre-treatment of mice with acute CORT failed to prevent neuroinflammatory responses to METH. Surprisingly, when mice were pre-treated with chronic CORT in the drinking water, an enhanced striatal neuroinflammatory response to METH was observed, an effect that was accompanied by enhanced METH-induced astrogliosis and dopaminergic neurotoxicity. Chronic CORT pre-treatment also sensitized frontal cortex and hippocampus to mount a neuroinflammatory response to METH. Because the levels of chronic CORT used are associated with high physiological stress, our data suggest that chronic CORT therapy or sustained physiological stress may sensitize the neuroinflammatory and neurotoxicity responses to METH.     

Fattening responses to daily intervals of heat exposure in the Syrian hamster

Warm ambient temperature (38 degrees C) provided daily for one hr induced time-dependent changes in body weight and fat stores in the Syrian hamster. In animals held on 10-hr daily photoperiods and room temperature (23 degrees C), daily one-hour thermopulses at 8 and 20 hr after light onset stimulated increases in body weights and indices of body fat storage. Abdominal fat pad weights of these groups were twice those of untreated controls after 17 and 28 days of thermoperiodic treatments. On the other hand, daily thermopulses were completely ineffective at 0 and 16 hr after light onset. These results demonstrate that body fat stores may be influenced by a temporal interaction of environmental stimuli and implicate underlying circadian mechanisms in the regulation of body fat.     

Haemodynamic and hormonal responses to heat exposure in a Finnish sauna bath

Eight healthy young men were studied during three periods of heat exposure in a Finnish sauna bath: at 80 degrees C dry bulb (80 D) and 100 degrees C dry bulb (100 D) temperatures until subjective discomfort, and in 80 degrees C dry heat, becoming humid (80 DH) until subjective exhaustion. Oral temperature increased 1.1 degrees C at 80 D, 1.9 degrees C at 100 D and 3.2 degrees C at 80 DH. Heart rate increased about 60% at 80 D, 90% at 100 D and 130% at 80 DH. Plasma noradrenaline increased about 100% at 80 D, 160% at 100 D and 310% at 80 DH. Adrenaline did not change. Plasma prolactin increased 2-fold at 80 D, 7-fold at 100 D and 10-fold at 80 DH. Blood concentrations of the beta-endorphin immunoreactivity at 100 D, adrenocorticotropic hormone (ACTH) at 100 D and 80 DH, growth hormone at 100 D and testosterone at 80 DH also increased, but cortisol at 80 D and 100 D decreased. The plasma prostaglandin E2 and serum thromboxane B2 levels did not change. Patterns related to heat exposure were observed for heart rate, plasma noradrenaline, ACTH and prolactin in the three study periods.     

Physiological responses of aged men to head-up tilt during heat exposure

The effects of age on cardiovascular and thermoregulatory responses to passive tilting were investigated using six old (61-73 yr) and 10 young (21-39 yr) unacclimatized men. Experiments were carried out at 26 degrees C and after exposure to 40 degrees C and 40% relative humidity for 105 min. Continuous measurements of esophageal (Tes) and mean skin (Tsk) temperatures and heart rate (HR) were recorded. Other variables studied included blood pressure (BP), forearm blood flow (FBF), and cardiac output (CO), which were measured at 4- to 5-min intervals. Measurements were made in the supine position and after 70 degrees head-up tilt for 15 min. Cardioacceleration during the tilt test was greater in the young men than in the old. Other cardiovascular responses of the old men to orthostatism were qualitatively similar to that of the young except for FBF and forearm vascular conductance. The old men did not show significant changes in FBF during tilting, suggesting a deterioration in the sympathetic nervous reflex in the aged. However, other circulatory adaptations seemed to overcome this deficiency resulting in orthostatic tolerance similar to that of the young. During head-up tilt at 26 and 40 degrees C, Tes of both age groups increased. This may reflect a decrease in conductive heat transfer presumably due to diminished blood flow to the periphery.