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At least 217 records · Page 12Linked to original sources
PubMed1992

A discrete mode of the antipyretic action of AVP, alpha-MSH and ACTH.

The antipyretic effect of AVP, alpha-MSH and ACTH consists in lowering the thermoregulatory threshold and in shortening the time span of the fever. Thus, neuropeptides influence activity of hypothalamic neurones regulating body temperature. This was confirmed by recent experiments of Moravec (this volume) which indicate that spontaneous activity and thermosensitivity of neurones in hypothalamic slices can be influenced, by AVP. Why neuropeptides of different chemical structure such as AVT, on one hand, and alpha-MSH and ACTH, on the other hand, induce the same effect on thermoregulation remains to be elucidated.

Adrenocorticotropic Hormone↗
PubMed1978

Effects of intravenous and intraventricular prostaglandin E1 on thermoregulatory responses in rabbits.

The thermal responses produced by both systemic and central administration of prostaglandin E1 (PGE1) at the three different ambient temperatures (Ta) of 2, 22 and 32 degrees C were measured to assess the possible involvement of PGE1 in temperature regulation. The body temperatures, metabolic rate, respiratory evaporative heat loss and vasomotor activity in response to PGE1 were measured. Intravenous administration of PGE1 produced dose-dependent hypothermia at Ta's of both 2 and 22 degrees C. The PGE1 hypothermia was due to cutaneous vasodilation. However, at a Ta of 32 degrees C, intravenous PGE1 produced no changes in rectal temperature and ear blood flow. On the other hand, the direct injection of PGE1 into the third ventricle produced dose-dependent hyperthermia. At a Ta of 22 degrees C, PGE1 fever was due to decreased heat loss along with a small increase in heat production. In the cold, PGE1 fever was due to increased heat production while in the heat heat losses were decreased. The data suggest that elevating PGE1 levels in the periphery causes a hypothermia, while elevating PGE1 levels in the central nervous system causes a hyperthermia at Ta's of both 2 and 22 degrees C.

Animals↗
PubMed2000

Effects of food deprivation on daily changes in body temperature and behavioral thermoregulation in rats.

Homeothermic animals regulate body temperature (T(b)) by using both autonomic and behavioral mechanisms. In the latter process, animals seek out cooler or warmer places when they are exposed to excessively hot or cold environments. Thermoregulation is affected by the state of energy reserves in the body. In the present study, we examine the effects of 4-day food deprivation on circadian changes in T(b) and on cold-escape and heat-escape behaviors in rats. Continuous measurement of T(b) during food deprivation indicated that the peak T(b) amplitude was not different from baseline values, but the trough amplitude continuously decreased after the onset of food deprivation. Cold-escape behavior was facilitated by food deprivation, whereas heat-escape behavior was unchanged. After the termination of food deprivation, the lowered T(b) returned to normal on the first day. However, cold-escape behavior was still facilitated on the third day after food reintroduction. Autonomic and behavioral thermoregulatory effectors are modulated in the face of food shortage so as to maintain optimal performance during the active period, whereas increasing energy conservation occurs during the quiescent phase.

Animals↗
PubMed1991

Regulation of body temperature, metabolic rate, and sleep in fasting pigeons diurnally infused with glucose or saline.

To test the hypothesis that nocturnal body temperature (Tb) and metabolic rate (MR) in the pigeon are regulated during sleep at levels proportional to energy reserves, continuous recordings of Tb, oxygen consumption (VO2), carbon dioxide production, and electrophysiological measures were taken from five pigeons subjected to two separate 4-day fasts. Energy reserves were depleted differentially during the fasts by 12-h diurnal infusions of either saline or isosmotic glucose solutions. Although Tb and VO2 were closely correlated, VO2 declined throughout the fast during diurnal and nocturnal phases of the 12:12 light-dark cycle whereas significant declines in Tb were restricted to the night. Diurnal thermal conductance declined over days of fasting, especially during saline infusions, and was reduced to minimal levels each night. The durations and distributions of arousal states did not change during the fast or differ between conditions. The results were consistent with the hypothesis of a nocturnal regulation of Tb and metabolic rate proportional to energy reserves.

Animals↗
PubMed1991

Differential influence of medial and lateral preoptic areas on body temperature in conscious and unconscious rats.

Since temperature sensitive neurons are unevenly distributed in the medial and the lateral preoptic areas, it was hypothesized that the two areas possibly would influence body temperature to a different extent. As alteration in sleep-wakefulness and body movement may affect the body temperature, experiments were conducted by reversible inactivation of those two areas, in freely moving (conscious) rats as well as in rats where changes in EEG and movement were restricted (unconscious). Results showed that the medial preoptic area is more effective in body temperature regulation. The study also revealed that the preoptic area mediated effect on body temperature regulation is not necessarily linked to simultaneous changes in sleep-wakefulness and alteration in the latter probably helps in maintaining the former within limit.

Anesthesia, General↗
PubMed1993

[Interleukin-1 beta and interleukin-6-plasma concentrations in laparotomies. Interaction with neuroendocrine secretion and postoperative temperature regulation?].

Elevated body temperature, increased plasma cortisol concentrations, and loss of the circadian secretory pattern are typical changes observed after trauma and surgery. We investigated the hypothesis that the interleukins IL-1 beta and IL-6 are involved in these phenomena, since both are endogenous pyrogens and can induce ACTH and cortisol secretion. METHODS. Eight healthy women undergoing hysterectomy for non-malignant diseases participated in the study after having given written consent. The study had the approval of our institution's ethics committee. Anaesthesia was induced with fentanyl 0.1 mg and methohexitone 1.5 mg/kg and maintained with isoflurane in 60% N2O and 40% O2. Blood samples were drawn before induction, before incision, during surgery, at the end of surgery, and 30, 60, 120, 240 and 360 min after surgery. Cortisol, prolactin, IL-1 beta, and IL-6 concentrations were determined with commercially available ELISAs. Statistical analysis was performed with non-parametric methods. RESULTS. IL-6 increased significantly from 15 (4.3-23) to 68 (18-107) pg/ml (medians and range) at the end of surgery and peaked at 128 (52-214) pg/ml 60 min postoperatively (p < 0.01, Table 2). Baseline IL-1 beta concentrations were 20 (1-35) pg/ml with a significant increase in median postoperative concentrations in the postoperative period (p < 0.001). Prolactin increased from 22 (13-43) to 210 (115-291) ng/ml immediately after induction of anaesthesia (p < 0.001) and remained elevated until 240 min after surgery. Cortisol increased from 99 (26-167) to 384 (241-553) ng/ml during surgery and reached a maximum of 475 (246-597) ng/ml 30 min postoperatively (Table 3). Rectal and mean body temperatures increased significantly in the postoperative period (Table 1). There was a significant correlation between IL-6 and cortisol concentrations (r = 0.468; p < 0.001), but none was found between IL-6 and temperature or between IL-1 beta and cortisol or temperature. CONCLUSIONS. Surgical trauma markedly stimulates the secretion of IL-6, and to a lesser extent that of IL-1 beta. The data do not yield any evidence indicating an effect of IL-1 beta or IL-6 on body temperature. Postoperative prolactin concentrations might be influenced by IL-6. The positive correlation between plasma concentrations of IL-6 and cortisol may be coincidental, but could reflect a causal relationship, particularly in the postoperative period during which time the circadian pattern of cortisol secretion is disturbed.

Body Temperature↗
PubMed2001

Hypothalamic cholinergic regulation of body temperature and water intake in rats.

Without disturbing the behavior of unanesthetized rats, the perfusion of neostigmine through microdialysis probe into the anterior hypothalamus (AH), paraventricular nucleus (PVN) and lateral ventricle (LV) decreased body temperature and increased water intake. On the other hand, the perfusion into the supraoptic nucleus (SON) increased the body temperature. The perfusion of neostigmine increased the extracellular concentration of acetylcholine in the perfusion sites except LV. Changes, both decrease and increase, in body temperature and increase in water intake were correlated with increases in c-fos-like immunoreactivity (Fos-IR) in the hypothalamus, pons and medulla. Distinct Fos-IR was found in the PVN, SON, median preoptic nucleus (MnPO), locus coeruleus (LC), area postrema and nucleus of the solitary tract (NTS). Co-administration of atropine with neostigmine completely suppressed the changes in the body temperature, water intake and Fos-IR, all of which were induced by the neostigmine perfusion into AH, PVN and SON. In the LV-perfused rats, on the other hand, co-administration of atropine and neostigmine only partially prevented body temperature reduction and still induced significant hypothermia. These results suggest that muscarinic receptor activation in specific regions of the hypothalamus and the activation of LC and NTS are implicated in the regulation of body temperature and water intake. Other receptor processes are involved in the LV-induced changes.

Animals↗
PubMed1990

Litorin and litorin-albumin conjugate as effective regulators of body temperature in rats.

Intraperitoneal injection of the bombesin-like peptide litorin (0.5 ml of a 10(-5) M solution) led to a short-lived decrease in the body temperature (maximum of 0.9 degrees C) of laboratory rats. In contrast, immunization with litorin conjugated to bovine serum albumin (BSA) led to an increase in body temperature from 36.6 +/- 0.1 to 37.2 +/- 0.1 degrees C that persisted for at least 4 weeks and which was probably due to the binding of endogenous litorin by the newly formed antibody. These results suggest that litorin is involved in the physiological regulation of thermal homeostasis. The temperature of control rats immunized with Freund's adjuvant and BSA without litorin fluctuated around normal at 36.6 +/- 0.1 degrees C over this period. Rat body weight increased evenly during the experiment in both the experimental animals and the two control groups. However, the volume of food intake in the hour following 24 h food deprivation was lower in rats immunized with conjugated litorin than in the control groups.

Animals↗
PubMed2005

Regulation of body temperature by thyrotropin-releasing hormone in neonatal chicks.

To understand thermal regulation of neonatal chicks, the contribution of thyrotropin-releasing hormone (TRH), a key regulator of the hypothalamus-pituitary-thyroid axis, was investigated. Intracerebroventricular (i.c.v.) injection of TRH (5 and 20 microg) increased body temperature, but did not change plasma T3 and T4 concentrations. Intraperitoneal (i.p.) injection of triiodothyronine (T3) and thyroxine (T4) did not influence body temperature. Thereafter, the relationships between TRH and the hypothalamus-pituitary-adrenal axis and sympathetic nervous system were further investigated. Central TRH stimulated both corticosterone and epinephrine release. The i.c.v. injection of a corticotropin-releasing factor receptor antagonist attenuated the change in body temperature and corticosterone concentration caused by TRH, but did not influence plasma T3 and T4 concentrations. The i.p. injection of epinephrine did not induce hyperthermia. Therefore, the thermoregulatory response to TRH may differ in neonatal stages being dependent upon the stimulation of the hypothalamus-pituitary-adrenal axis rather than the hypothalamus-pituitary-thyroid axis.

Animals↗
PubMed1999

Esophageal temperature threshold for sweating decreases before ovulation in premenopausal women.

The purpose of this study was to test the hypothesis that regulated body temperature is decreased in the preovulatory phase in eumenorrheic women. Six women were studied in both the preovulatory phase (Preov-2; days 9-12), which was 1-2 days before predicted ovulation when 17beta-estradiol (E2) was estimated to peak, and in the follicular phase (F; days 2-6). The subjects walked on a treadmill ( approximately 225 W x m-2) in a warm chamber (ambient temperature = 30 degreesC; dew-point temperature = 11.5 degreesC) while heavily clothed. E2, esophageal temperature (Tes), local skin temperatures, and local sweating rate were measured. The estimate of when the E2 surge would occur was correct for four of six subjects. In these four subjects, E2 increased (P </= 0.05) from 42.0 +/- 24.5 pg/ml during F to 123.2 +/- 31.3 pg/ml during Preov-2. Resting Tes was 37.02 +/- 0.20 degreesC during F and 36.76 +/- 0.28 degreesC during Preov-2 (P </= 0.05). The Tes threshold for sweating was decreased (P </= 0.05) from 36.88 +/- 0.27 degreesC during F to 36. 64 +/- 0.35 degreesC during Preov-2. Both mean skin and mean body temperatures were decreased during rest in Preov-2 group. The hypothesis that regulated body temperature is decreased during the preovulatory phase is supported.

Adult↗
PubMed1979

Protein deficiency: its effects on body temperature in health and disease states.

Little is known about the effects of protein malnutrition on the ability to regulate body temperature during health and disease. To investigate this area, we placed young rabbits on a low-protein diet and recorded their body temperatures. There were no differences between the protein-deprived and control animals concerning their abilities to maintain constant body temperatures during exposure to low (5 C, 10 C) and thermoneutral ambient temperature (20 C). In a warm ambient temperature (30 C) the protein-deprived animals were actually better able to maintain a lower body temperature. Injections with heat killed bacteria led to little or no fever in the protein-deprived group. However, intravenous injections of endogenous pyrogen, a protein mediator of fever, resulted in fevers virtually identical to that attained in control animals. These data indicate that the attenuated febrile response to bacterial injection during protein deprivation may be due to a diminished production of endogenous pyrogen, and not to some alteration in the central nervous system sensitivity to pyrogens.

Animals↗