Ambient temperature-dependence of sleep disturbances produced by basal forebrain damage in rats

Amounts of sleep and waking were determined in rats at ambient temperatures (Ta's) of 20, 25, and 30 degrees C, before and after basal forebrain lesions. Rats were hyposomniac at all Ta's for 1-2 days postlesion. After that, sleep was highly Ta-dependent. Rats were typically hyperthermic after complete ablation of the medial preoptic area (MPOA), and the Ta at which maximal amounts of rapid-eye movement sleep (REMS) occurred frequently shifted from 30 to 25 degrees C. During the first postlesion month, amounts of slow-wave sleep (SWS), REMS, total sleep time ( TST ), and the proportion of time spent in REMS to TST (REMS/ TST ) all improved significantly at the Ta's at which the most REMS occurred (high REMS temperatures). In contrast, at the Ta's at which the least REMS occurred, these variables were as depressed one month after MPOA damage as they were at 5 days postlesion. REMS/ TST recovered most rapidly, returning to prelesion levels at high REMS temperatures within the first postlesion week. REMS bout durations were severely shortened after forebrain damage, and this was the only sleep disturbance not attenuated at high REMS temperatures. After smaller basal forebrain lesions, initial deficits were less severe and normal amounts of sleep returned earlier. However, as was the case for large lesions, sleep deficits were most severe and persistent at low REMS temperatures.     

Effects of exposure to hot environments on the regional distribution of blood flow and on cardiorespiratory function in sheep

Summary Sheep were exposed to thermoneutral conditions and then to either mild heat stress (40° C dry bulb/26° C wet bulb temperature) or to severe heat stress (42/39° C). The following measurements were made: regional distribution of cardiac output, deep body and skin surface temperatures, respiratory frequency, heart rate, blood pressure, cardiac output, oxygen consumption, haemoglobin concentration, theP _{CO 2},P _{O 2}, pH,S _{O 2} andC _{O 2} of arterial, mixed venous, dorsal sagittal sinus and transverse sinus blood. Body temperature and heart rate increased, and panting resulted in a marked respiratory alkalosis during severe heat stress, but otherwise, changes in gross cardiorespiratory functions were small. During both mild and severe heat stress approximately 11% of the cardiac output passed through arteriovenous anastomoses, compared with approximately 1.5% under thermoneutral conditions. Changes in blood flow to the skin, nasal mucosa and turbinates, tongue, heart, thyroids, adrenals, gut, spleen, kidneys, skeletal muscle, brain and spinal cord, illustrate a redistribution of cardiac output appropriate to combat the heat stress, but with probable influences of the respiratory alkalosis and alterations in local tissue metabolic rate.     

Cytokines and Thermoregulation: Interleukin-9 Injected in preoptic area fails to evoke fever in rats

A number of the members of the family of cytokines including IL-1, IL-2, IL-6, and IL-11 act directly in the brain to induce a febrile response in the rat and other species. The purpose of this study was to examine the effect of interleukin-9 (IL9) when this cytokine is applied directly to the thermosensitive and pyrogen reactive region of the anterior hypothalamic, preoptic area (AH/POA). In male Sprague-Dawley rats, guide cannulae for microinjection into the AH/POA were implanted stereotaxically, and radio transmitters for monitoring body temperature (T_b) were placed intraperitoneally. Following postoperative recovery, recombinant murine macrophage inflammatory protein (MIP)-1β was microinjected in the AH/POA of each rat in a dose of 28 pg/1μl to identify pyrogen reactive sites in the AH/POA. Then recombinant human IL-9 was suspended in pyrogen-free CSF vehicle and microinjected in the same sites in concentrations of 2.4, 24, and 240 U/μl. In contrast to the pyrexic action of MIP-1β, IL-9 failed to elicit a significant alteration in the T_b of the rats at any of the doses tested. IL-9 was also without effect on the intakes of either water or food. These results demonstrate that IL-9 applied to the region of the diencephalon in which other cytokines act to evoke fever may not play a direct role in the thermogenic component underlying the acute phase response. However, as demonstrated in several different cell systems, IL-9 may require a cofactor related to pyrogen for a febrile response to develop.     

Lesions of periventricular tissue surrounding the anteroventral third ventricle (AV3V) attenuate salivation and thermal tolerance in response to a heat stress

The purpose of this study was to determine if ablation of the periventricular tissue that surrounds the anteroventral third ventricle (AV3V) would reduce an animal’s ability to withstand a thermal challenge. The results show that AV3V-lesion rats are less capable of withstanding a 37 °C heat stress and that this is, at least in part, due to a reduced salivation response.     

Hyperthermic response of the cat to intraventricular injection of the opioid delta-receptor agonist D-Ala2-D-Leu5-enkephalin

The delta opioid receptor agonist D-Ala2-D-Leu5-enkephalin was injected into the third cerebral ventricle of cats to determine its effects on core temperature for comparison with other peptide and non-peptide opioids that act on a variety of receptors to alter thermoregulation. Like other opioid peptides that have been studied in this species, D-Ala2-D-Leu5-enkephalin (5-25 micrograms) induced a dose-related hyperthermia. This response was undiminished in cats tolerant to morphine and was found to consist of two components. One component of the hyperthermic response was inhibited by pretreatment with low doses of opioid antagonists (25 micrograms naloxone; 5-15 micrograms naltrexone) and may be mediated by the v2-receptor that mediates this response to D-Ala2-Met-enkephalinamide. The other component, which was prevented by 100 micrograms naltrexone but still only partially inhibited by 250 micrograms naloxone, is attributed to delta-receptor stimulation. In tests over a range of environmental temperatures, the hyperthermic response to 10 micrograms D-Ala2-D-Leu5-enkephalin was less in a 4 degrees C environment than at the usual laboratory temperature of 22 degrees C. Responses in 22 and 34 degrees C environments were similar. No increase in respiratory rate occurred to indicate activation of compensatory heat-loss mechanisms so that the hyperthermia was indicative of an increase in the level about which body temperature is regulated.     

Effects of environmental temperature on the development of a noradrenergic thermoregulatory mechanism in the rat

Rats reared at 30°C do not exhibit the same thermoregulatory competence during cold exposure as do rats reared at 20° C. They are even more clearly distinguished by the absence of an hypothermic response to intrahypothalamic noradrenaline (IH-NA). In one series of experiments, different groups of rats all received 120 days 30° C-exposure and 20 days 20° C-exposure. The 20° C-exposure occurred at different ages in different treatment groups. At 140 days of age, bilateral IH-NA injections (each 10 g/1 l CSF) were administered in conscious rats and the body temperature response observed. An hypothermic response to IH-NA was observed in groups whose exposure to 20° C terminated between 20 and 80 days of age. In a second series of experiments, duration of rearing at 20° C varied but always started at 40 days of age. Responses to IH-NA in 140-day-old adults indicated that the exposure required to induce 50% of the hypothermic response of control (20° C-reared) rats was 17days. These data suggest that there is an hypothalamic noradrenergic mechanism implicated in the control of body temperature whose development is affected by environmental temperature in a duration-dependent manner. The period during which this effect may be exerted extends into adulthood.     

Temperature preferences and the effect of changes in serotonin in maturing mice

Behavior of maturing mice in a 20 cm long thermal gradient is described. Mean preferred temperatures (T_pref) under standard test conditions ranged from about 29° to 31° in untreated mice aged 3, 7, 10, and 14 days postpartum, which is similar to the temperature maintained in the nest by parent mice. Increased serotonin (5-HT) after injection of the precursor 5-hydroxytryptophan (30 mg/kg) was generally associated with increasted T_pref (7 and 10 days) as compared with vehicle injected littermate controls in a double-blind study. Depletion of 5-HT following p-chlorophenylalanine (400 mg/kg) was associated with decreased T_pref (3 and 7 days). Relationships with body temperature and thermoregulation are discussed and handling cautions are presented.     

Naltrexone-induced hypothermia in the rat.

Naltrexone, in relatively high doses, has been reported to cause a fall in body temperature in human ex-heroin addicts who had been abstinent for at least 6 weeks. The underlying mechanism of this hypothermic effect has been investigated in rats. The first consideration was that the temperature change was a reflection of delayed withdrawal but rats implanted with a morphine pellet 45 days earlier showed no significant change in temperature after a dose of naltrexone that caused marked withdrawal hypothermia in dependent rats implanted 3 days previously. A fall in core temperature was only induced in rats after doses of 80 and 160 mg/kg i.p. of naltrexone. Behavioral thermoregulatory studies revealed that the animals correct the falling body temperature by increased exposure to a radiant heat source indicating that the central thermostats had not been significantly affected by the drug. These data suggest that the major component in the hypothermic effect of naltrexone is activation of efferent heat loss pathways or peripheral heat loss mechanisms. Due to current suggestions that opiate receptors might represent the receptors for an endogenous transmitter the results are discussed in relation to this consideration. When compared to the sites and mechanism of action of opiates on thermoregulation the results with naltrexone lend little support to the hypothesis that the fall in temperature is due to displacement of an endogenous substance from central opiate receptors.     

Incubators versus mothers' arms: body temperature conservation in very-low-birth-weight premature infants

OBJECTIVE: To determine whether there is a significant difference between the temperatures of very-low-birth-weight (VLBW) premature infants in the incubator and in the mothers' arms. DESIGN: Repeated measures, with random assignment to treatment order and the infants serving as their own controls. SETTING: A 40-bed tertiary-level nursery in a university teaching hospital. PARTICIPANTS: A convenience sample of 20 preterm infants weighing 1,095 to 1,500 g and from 30 to 37 weeks postconceptional age. The infants were screened for factors that would interfere with temperature maintenance. MAIN OUTCOME MEASURES: Axillary temperatures were measured with an electronic thermometer for equal periods of time in incubators and mothers' arms. The mean temperature differences between the two study conditions were compared using two-tailed t tests and repeated analysis of variance (ANOVA). Weight was monitored and analyzed for evidence of increased metabolic activity. RESULTS: No significant variations were found in the infants' mean temperatures in the incubator, but the infants were significantly warmer while in their mothers' arms. CONCLUSION: VLBW premature infants can maintain a stable temperature in their mothers' arms without evidence of increased metabolic activity. Nurses can encourage mothers to hold their infants without fear of cold stress or weight loss.     

Postoperative shivering

Shivering ist ein h?ufig beobachtetes und seit langem bekanntes Problem in der postoperativen Phase. Es handelt sich um unwillkürliches Muskelzittern und eine Erh?hung des Muskeltonus als Gegenregulation des Organismus im Sinne eines Abwehrmechanismus bei einem Abfall der Ist-Temperatur gegenüber dem Temperatursollwert. Die H?ufigkeit wird in der Literatur sehr unterschiedlich mit 5–65% angegeben [11]. Shivering ist nicht nur ein für den Patienten subjektiv sehr unangenehmes Ph?nomen – einige Patienten erinnern es als das Unangenehmste an der gesamten Operation – sondern birgt insbesondere für kardial und pulmonal vorerkrankte Patienten deutliche Risiken. Ursache hierfür ist der beim Shivering erh?hte Energie- und damit auch Sauerstoffverbrauch des Patienten. Wesentliche Erkenntnisse über das Ph?nomen des Shivering und der Mechanismen der Thermoregulation unter An?sthesie verdanken wir der Arbeitsgruppe um Daniel Sessler.

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