Fall In Rectal Temperature Research Articles

Prone sleeping infants have a reduced ability to lose heat.

The heat loss coefficients of a group of infants have been calculated and compared to see if there is a difference in the ability to lose heat between prone and non-prone sleeping infants. For a group of 43 infants aged 4-29 weeks, a simple mathematical model of exponential cooling in a body has been fitted to the fall in rectal temperature which occurs in infants at bedtime. One of the parameters yielded by the fitting process is the coefficient of thermal heat loss. After validation against the estimated heat loss from supine sleeping infants, the heat loss coefficient was compared at different sleep positions and gender. The mean heat loss coefficient, measured from the non-prone sleeping infants (0.269 W/degrees C, S.D. 0.197) agreed well with the value calculated for supine sleepers with the same tog levels (0.4 W/degrees C). Prone sleeping infants were found to have a considerably smaller heat loss coefficient which was approximately 60% of the value for non-prone sleeping infants (P = 0.000097). Female infants were found to have a heat loss coefficient that was approximately 70% of that of male infants but this gender difference was only significant (P = 0.025) for non-prone sleeping infants. These results suggest that infants sleeping in the prone position may be unable to lose heat as rapidly as those infants sleeping non-prone.

Effects of repeated exposures to severely cold environments on thermal responses of humans.

This study was conducted to investigate the effects of different exposure rates on thermal responses with the total cold exposure time the same under each of the conditions. After resting in a warm room (25 degrees C) for 10 minutes, six male students wearing standard cold protective clothing entered an adjoining cold room (-25 degrees C). Each 5-, 10- and 20-minute cold exposure was repeated 12, 6 and 3 times, respectively. Each cold exposure was followed by a similar duration of rest at 25 degrees C. Total cold exposure time was the same under the three conditions. Rectal temperature, skin temperatures, blood pressure, 17-hydroxycoyticoids (OHCS), counting task and subjective responses were measured. At the end of the cold exposure skin temperatures in the shorter exposures were higher than those in the other conditions, except on the foot. Discomfort due to cold was less in the shorter exposures and manifestation of discomfort was delayed. However, there were no differences among the three conditions in the fall of rectal temperature and urinary excretion of 17-OHCS, which are good indices of cold stress. Moreover, increase in blood pressure and decrease in counting task due to cold were not different among the three conditions. Even though the cold exposure time for each stay was short, when cold exposures were repeated frequently, cold stress of the whole body and decrease in manual task performance were the same as in the longer cold exposure.

5-HT 1D receptors mediate SKF 99101H-induced hypothermia in the guinea pig

The selective, brain penetrant, 5-HT(1D) receptor agonist SKF 99101H (10-30 mg/kg i.p.) caused a dose-related fall in rectal temperature in guinea pigs which lasted longer than 2 h. Sumatriptan (1.0-100 mg/kg i.p.), a selective 5-HT(1D) agonist which does not penetrate the brain, did not produce hypothermia, suggesting that peripheral mechanisms are not critically involved in the response. The hypothermia induced by SKF 99101H (30 mg/kg i.p.) was dose-dependently blocked by the 5-HT(1D) receptor antagonists GR 127935 (0.01-1 mg/kg i.p.) and GR 125743 (0.01-3 mg/kg i.p.), confirming the role of 5-HT(1D) receptors. Mianserin (0.3-10.0 mg/kg i.p.) and granisetron (0.1-3.0 mg/kg i.p.) were inactive, suggesting that 5-HT(2A/2B/2C) or 5-HT( 3) receptors play no significant role in the generation of the hypothermic response. Nor was the hypothermia reversed by prazosin (0.03-1.0 mg/kg i.p.), idazoxan (0.03-1.0 mg/kg i.p.) or scopolamine (0.01-0.3 mg/kg i.p.), thereby excluding mediation by α(1)- and α(2)-adrenoceptors and muscarinic receptors. WAY 100635 (0.1-1.0 mg/kg) significantly potentiated the effect of SKF 99101H. The antagonists, when given alone, had no effect on body temperature, with the exception of prazosin (0.1 and 1.0 mg/kg). Three days of treatment with parachloroamphetamine (30 mg/kg i.p.) depleted forebrain 5-HT by ∼ 75% in frontal cortex, hypothalamus, hippocampus and striatum, but failed to alter the hypothermic response to SKF 99101H. The hypothermia is, therefore, unlikely to be mediated by 5-HT(1D) receptors located on 5-HT neurons. SKF 99101H-induced hypothermia in the guinea pig may serve as a useful model for investigation of centrally acting 5-HT( 1D) receptor antagonists.

Pentoxifylline decreases body weight loss and muscle protein wasting characteristics of sepsis.

Sepsis induces metabolic disorders that include loss of body weight, muscle wasting, and acute-phase protein synthesis in liver. Cytokines are generally recognized as active mediators of these disorders, and the implication of tumor necrosis factor (TNF) has been frequently discussed in the recent past. However, the identity of the active agent in alterations of protein metabolism is still controversial. To improve our understanding of the role of cytokines in mediating muscle wasting observed in sepsis, we investigated muscle and liver protein metabolism in the following three groups of rats: infected control rats (INF-C); infected rats pretreated with pentoxifylline (PTX-INF), which is a potent inhibitor of TNF secretion; and pair-fed rats for the PTX-INF group pretreated with pentoxifylline. Pentoxifylline nearly completely suppressed TNF secretion but did not influence the transient fall in rectal temperature, the decreased hematocrit, and the increased liver protein mass and synthesis observed in INF-C rats. Pentoxifylline decreased the anorexia, the loss of body weight and muscle protein observed in INF-C animals, and partially prevented the decrease in muscle protein synthesis induced by infection. The overall data indicate that pentoxifylline is an effective agent in mitigating the characteristic muscle protein wasting induced by sepsis and confirm the limited role of TNF in the mediation of the acute-phase protein synthesis. Our results suggest a probable implication of TNF in the regulation of protein balance in muscle but do not allow discarding possible implication of other mediators that would be inhibited by pentoxifylline.

Test of a quick-don wet immersion suit for off-shore use

Tests of “Spacetime” Survival Coverall suits and the associated gloves and boots of the ensemble were carried out on six men. Four men maintained their rectal temperature above 36°C for six hours in a bath of circulating water at 12°C. Two men had to be withdrawn from the bath because they reached a rectal temperature of 35.5°C, the ethical withdrawal criterion, before the six-hour period had elapsed. Linear regression of rectal temperature versus time during the terminal part of the exposure was carried out for all men. One of the subjects who was withdrawn would almost certainly have had a rectal temperature above 34°C at the end of six hours had he remained in the bath. The other subject would have had a rectal temperature classifiable as “incipient death” (30°C). The relatively rapid fall in rectal temperatures in two subjects did not appear to relate directly to body size, but leakage may have been a contributing factor. Comparison with data in the literature indicates that the immersion suit is advantageous, but separate experimentation would have to be carried out to determine quantitatively how valuable it is in extending the survival time of men immersed in cold water in comparison with other suits on the market.

Thermoregulation and afterdrop during hypothermia in patients with poikilothermia

The pathophysiology of afterdrop of core temperature during rewarming in patients with induced or accidental hypothermia remains controversial. We studied the effect of cooling and rewarming in four female patients with acquired poikilothermia and in four normal females. Exposure to cold air (16.5 degrees C) induced shivering and adequate vasoconstriction in normal individuals, without a fall in rectal temperature (Tr; 36.3 +/- 0.2 degrees C [mean +/- SD]); subsequent heating (40 degrees C) induced a rise in Tr to 37.0 +/- 0.3 degrees C and generalized sweating. The four patients all had spontaneous hypothermia (Tr 34.1 +/- 0.9 degrees C) before cooling. Tr decreased by 0.3-0.9 degrees C during cold exposure, and a marked afterdrop of Tr (0.3-0.5 degrees C) occurred during rewarming: this did not occur in normal individuals. Cooling failed to induce shivering and vasoconstriction in three patients. No patient showed visible sweating during heating despite a Tr of up to 38.0-38.5 degrees C and skin temperature of up to 37.7-38.5 degrees C. The basal metabolic rate was decreased by 71-82% in all patients during steady-state hypothermia and remained lowered during normothermia in two patients. We conclude that during hypothermia three of the four patients showed severe disorders of peripheral vasomotor function and shivering response. These data provide evidence for thermal conduction as the major mechanism of afterdrop during hypothermia.

Indomethacin (Confortid) in severe head injury and elevated intracranial pressure (ICP).

In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control ICP by hyperventilation and barbiturate sedation, indomethacin (Confortid) was used as a cerebral vasoconstrictor drug. In all patients indomethacin reduced ICP to below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in cerebral blood flow (CBF) at 2 hours. After 7 hours, ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In two patients a return of ICP and CBF to pretreatment levels was observed. In all patients indomethacin treatment was followed by a fall in rectal temperature. Outcome scaling has not yet been performed, but all patients left hospital without neurological deficits. The results suggest, that indomethacin is an alternative in the treatment of ICP-hypertension in head-injured patients.

The effects of indomethacin on intracranial pressure, cerebral blood flow and cerebral metabolism in patients with severe head injury and intracranial hypertension

In five head-injured patients with cerebral contusion and oedema in whom it was not possible to control intracranial pressure (ICP) (ICP greater than 20 mmHg) by artificial hyperventilation (PaCO2 level 3.5-4.0 kPa) and barbiturate sedation, indomethacin was used as a vasoconstrictor drug. In all patients, indomethacin (a bolus injection of 30 mg, followed by 30 mg/h for seven hours) reduced ICP below 20 mmHg for several hours. Studies of cerebral circulation and metabolism during indomethacin treatment showed a decrease in CBF at 2 h. After 7 h, ICP remained below 20 mmHg in three patients, and these still had reduced CBF. In the other patients a return of ICP and CBF to pretreatment levels was observed. In all patients indomethacin treatment was followed by a fall in rectal temperature. These results suggest that indomethacin due to its cerebral vasoconstrictor and antipyretic effect should be considered as an alternative for treatment of ICP-hypertension in head-injured patients.

After two weeks habituation to capsaicinized food, rats prefer this to plain food

In a first series of experiments rats were accustomed for two weeks to eat chow with capsaicin (250 micrograms: 1 g of food). After this habituation period, when free to choose, 3 rats out of 4 preferred eating the piquant chow. In a second series of experiments the rats had access to a choice of chows without any habituation period. In this series, the choice between piquant and nonpiquant chow showed that 4 rats out of 5 preferred to eat the chow without capsaicin. The present experiment shows that the piquant chow eaten by rats produced a fall in rectal temperature 48 h later. The present experiment provides some evidence that rats accustomed to eat piquant food manifested, when free to choose, a preference for an innately unpalatable piquant chow.

Porcine Malignant Hyperthermia

Malignant hyperthermia (MH) can be triggered in swine either by stress or by certain anesthetic agents. In humans, MH commonly occurs in patients previously exposed uneventfully to triggering anesthetics. This variability in expressivity of the MH syndrome is a combination of unknown genetic and environmental factors. A hypothesis was tested that a fall in rectal temperature following general anesthesia can prevent the MH syndrome in susceptible patients. Nine littermate Pietrain pigs with MH were exposed to halothane after their rectal temperatures were stabilized at 35 degrees, 36 degrees, and 37 degrees C during thiopental/nitrous oxide anesthesia. The in vivo MH metabolic, cardiopulmonary, and contracture responses were attenuated at the lower rectal temperatures. The effect of varying temperatures on biopsies of skeletal muscle from these animals showed a marked decrease in contracture response to halothane when the muscle was cooled to 25 degrees C. Studies on the Ca2+ uptake process and on Ca2+ channel-Ca2+ release properties of isolated sarcoplasmic reticulum (SR) membranes showed that increasing incubation temperatures from 25 degrees to 38 degrees C increased the Ca2+ uptake rate by the SR Ca2+ pump and also increased the probability of Ca2(+)-induced Ca2+ opening of a Ca2+ channel and the release of stored Ca2+. This study indicates that temperature can have a marked effect on the expressivity of the MH defect at the whole animal, isolated tissue, and fragmented membrane levels of organization. Since many surgical patients' temperatures decrease after induction and anesthesia, this may explain one environmental factor that determines the incidence, rate, and magnitude of the MH syndrome.

Hypothalamic somatostatin may mediate endotoxin-induced fever in the rat

(1) The changes in rectal temperature produced by an injection of a bacterial endotoxin piromen (10-40 ng in 1.0 microliter) on somatostatin-14 (SS-14; 0.1-0.3 microgram in 1.0 microliter) into the preoptic anterior hypothalamic area were assessed and compared in control rats, in rats with hypothalamic SS depletion, and in rats with hypothalamic SS receptor blockade. (2) Intrahypothalamic injection of either piromen or SS-14 produced a dose-related rise in rectal temperature in intact, control rats. The fever induced by intrahypothalamic injection of piromen or SS-14, as well as that induced by intraperitoneal injection of piromen, was antagonized by pretreatment of the hypothalamus with a SS-14 receptor antagonist (0.1 ng in 1.0 microliter) in rats. (3) On the other hand, intraperitoneal administration of cysteamine (30-100 mg/kg), in addition to producing a dose-related fall in rectal temperature, also caused a dose-related fall in hypothalamic SS-levels in rats. Furthermore, the fever induced by intrahypothalamic injection of piromen, but not SS-14, was antagonized by depletion of hypothalamic SS levels with an intraperitoneal dose of cysteamine (30 mg/kg). (4) The results indicate that a somatostatinergic pathway in the hypothalamus may mediate endotoxin-induced fever in the rat.

Temperature and metabolic changes in rats after various doses of tumour necrosis factor alpha.

1. Sub-lethal doses of recombinant of tumour necrosis factor alpha (TNF alpha) were administered i.v. to young conscious male Wistar rats. Temperature changes and alterations in serum zinc and albumin concentrations and weight and composition of liver, kidney, spleen, tibialis muscle and skin were measured. Temperatures were monitored for 8 h and tissue parameters 8 and 22 h post-injection. 2. Doses above 10 micrograms/kg caused fevers of increasing magnitude and duration with latencies of 2 h. At doses of 200 micrograms/kg or more fevers were preceded by a fall in rectal temperature of up to 1.1 degrees C. 3. Weight loss by skin and tibialis and gain by liver occurred 22 h post-injection. Spleen and kidney weight and zinc and spleen protein contents were unaffected. Serum albumin and zinc fell 22 and 8 h after injection respectively. Liver zinc was elevated at both times and inversely correlated at 8 h with serum values. A degree of dose dependence of zinc and albumin changes existed. A gain in protein was evident in liver 8 h post-injection and a loss by muscle at 22 h. Paradoxical effects were observed in skin protein concentration. 4. TNF alpha mimicked many of the metabolic effects of E. coli endotoxin reported in the literature and showed similar effects to those described for interleukin 1 (IL1).

Effects of urethane, ambient temperature and injection route on rat body temperature and metabolism due to endotoxins.

1. We have investigated the influence of environmental temperature, anaesthesia and route of administration on rectal temperature and other metabolic responses to two preparations of bacterial endotoxin in male adult Wistar rats. 2. Urethane anaesthesia, environmental temperatures of 20 and 28 degrees C, subcutaneous (S.C.) and intraperitoneal (I.P.) routes of administration and butanol and trichloroacetic acid (TCA) extracts of E. coli endotoxin (1.2 mg/kg) were used. 3. In addition to rectal temperature, serum zinc, albumin and urea concentrations and liver protein, RNA and zinc contents were measured. 4. Fevers were produced by injections of both endotoxins, by either route at 28 degrees C. Butanol-extracted endotoxin produced a more rapid response than the TCA extract via the I.P. route whereas the TCA extract produced a higher temperature than the butanol extract when the S.C. route was used. 5. Fevers were inhibited at an environmental temperature of 20 degrees C and by anaesthesia, while the former had no effect on compositional changes the latter inhibited the fall in serum zinc in response to subcutaneous doses of either endotoxin and the increase in liver zinc content in response to the butanol extract of endotoxin. 6. At 20 degrees C a marked fall in rectal temperature occurred in conscious rats 2 h after receiving the TCA but not the butanol extract of endotoxin. Temperature depression was more severe when endotoxin was administered by the I.P. route. 7. Serum urea was elevated in conscious rats by the TCA extract of endotoxin via both routes but only by the I.P. route for the butanol extract of endotoxin. In anaesthetized animals only the TCA extract of endotoxin raised serum urea concentration when given intraperitoneally. 8. Serum albumin and liver protein and RNA were unaffected by endotoxin injections over the 7 h time course of the study. 9. Rectal temperature responses to endotoxins were influenced in direction and magnitude by all variables employed in the study, while compositional changes were unaffected by environmental temperature but influenced to varying degrees by urethane anaesthesia and the route of administration employed.

Anaphylactic shock-induced conditioned taste aversion: II. Correlation between taste aversion and indicators of anaphylactic shock

Previous studies (V. J. Djurić, B. M. Marković, M. Lazarević, & B. D. Janković, 1987, in B. D. Janković, B. M. Marković, & N. H. Spector (Eds.), Neuroimmune interactions, pp. 561–568, New York: New York Acad. Sci.; B. M. Marković, V. J. Djurić, M. Lazarević, & B. D. Janković, 1988, Brain Behav. Immun. 2, 11–23) have shown that rats learn to associate the taste of saccharin with the induction of anaphylactic shock, thus exhibiting conditioned taste aversion (CTA) toward an otherwise preferred saccharin solution. The present experiment investigates the effect of unconditioned stimulus intensity (the amount of antigen used for the induction of shock) on CTA. Rats were sensitized to ovalbumin and subjected to a conditioning trial in which the conditioned stimulus (CS; saccharin solution given orally) signaled the presentation of the unconditioned stimulus (US; shocking doses of ovalbumin ranging from 0.5 to 3 mg given intraperitoneally). Behavioral signs, hematocrit, and rectal temperature were used for evaluation of anaphylactic shock. Twenty-four hours after the conditioning trial, rats were subjected to a two-bottle preference test between saccharin solution and water. Multiple regression statistical analysis revealed significant correlations among saccharin preference ratio, dose of antigen used for the induction of shock, behavioral signs of shock, rise in hematocrit, and fall in rectal temperature. A dose-dependent relation among saccharin preference ratio and physiological indicators of shock suggests that conditioned anaphylactic shock-induced avoidance behavior is functionally related to homeostatic factors involved in immune reactivity.

Effects of intrathecal capsaicin on autonomic and behavioral heat loss responses in the rat

Capsaicin and Tween 80 were injected into the lumbar subarachnoid space of rats via a chronic cannula, and the thermoregulatory effects compared. The rats were placed in a climatic chamber at an ambient temperature (T a) of 20 and 30°C. In the first series of experiments the rats had no access to the fan lever. Intrathecal (IT) capsaicin injection produced a fall in rectal temperature, with a rise in cutaneous temperatures due to vasodilation. On the contrary, IT or the intraperitoneal (IP) Tween 80 injection route had no effect on body temperature. In addition capsaicin-administered IP induced a fall in spinal cord temperature (T sp). In the second series of experiments the rats had access to a lever activating a fan that drew cool outside air into the climatic chamber. After IT capsaicin injection, the rats increased bar-pressing behavior for fresh air. This was significant at both T a 20 and 30°C. The results tend to support the hypothesis of capsaicin action somewhere on the thermal afferent pathways. Furthermore, it is possible that the action of capsaicin on thermoregulatory behavior is mediated by the release of substance P from primary afferent terminals.

Effects of cholinesterase reactivators and atropine on fenitrothion-induced hypothermia in bubal us bubalis

Oral administration of fenitrothion (435 mg/kg) produced a pronounced fall in rectal temperature and erythrocyte AChE activity in buffalo calves. Treatment with DAM alone or in conjunction with atropine at the time of severe toxicity (within l h) significantly ( P < 0.01) reversed fenitrothion-indueed hypothermia and AChE inhibition. The temperature decrease and AChE inhibition were not significantly ( P > 0.05) altered by either 2-PAM or atropine. It is concluded that DAM may be more effective than either 2-PAM or atropine in reversing hypothermie effect of OP insecticides.

Effects of opiod antagonists and their quaternary analogs on temperature changes in morphine-dependent rats

Subcutaneous administration of three opioid antagonists; naloxone, naltrexone and nalmefene, produced a significant rise in tail skin temperature and a subsequent fall in rectal temperature in morphine dependent rats. However, subcutaneous administration of equimolar concentrations of the quaternary derivatives of these opioid antagonists (naloxone methobromide, naltrexone methobromide and n-methylnalmefenium iodide) failed to produce any significant alterations in either tail skin or rectal temperatures in the morphine dependent rat. At doses of naloxone methobromide 6 to 9 times greater than naloxone, there was a slight reduction of rectal temperatures with no significant elevation of skin temperature However, the fall in reactal temperature was still significantly less than that achieved with administration of naloxone. When each of these six agents were administered centrally (20 ug/5 ul, icv) in the morphine dependent rat, similar increases in tail skin temperature and decreases in rectal temperature were observed. These temperature changes were similar to those observed following systematic administration of the opioid antagonist. Previously, we have suggested that acute withdrawal in the morphine-dependent rat may serve as an animal model for the mechanism of the menopausal hot flush. Collectively, these results suggest that the temperature changes associated with morphine-withdrawal in our rat model for studying the mechanisms of the menopausal hot flush are centrally mediated.

Effects of bombesin on thermoregulatory responses and hypothalamic neuronal activities in the rat.

Direct administration of bombesin (1, 10, and 100 ng/microliter) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures (Ta) of 8 and 22 degrees C. The hypothermia in response to bombesin was brought about by a decrease in metabolism at Ta 8 degrees C, whereas at Ta 22 degrees C the hypothermia was brought about by both a decrease in metabolism and an increase in cutaneous temperature. However, at Ta 30 degrees C, intrahypothalamic administration of bombesin caused an insignificant change in thermoregulatory responses. On the other hand, 51 single neurons in the preoptic anterior hypothalamic area were examined in 20 rats under urethan anesthesia. Each animal was subjected to scrotal warming or cooling and to the administration of bombesin. Microiontophoretic application of bombesin resulted in inhibition of the majority (62.5%) of cold-responsive neurons as well as excitation of the majority (50%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (74%) of thermally unresponsive neurons were not affected by bombesin application. The data indicate that bombesin, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.

Circadian rhythm of rectal temperature in the blind

Abstract Attempts were made to compare the circadian rectal temperature rhythm between 5 blind and 5 sighted subjects. Rectal temperature was measured continuously for 24 h, at an ambient temperature of 28°C and a relative humidity of 60%, in the resting subject. The difference between the maximum and the minimum values of the rectal temperature (= range of oscillation) was 0.82 ± 0.09°C (mean ± S.E.) and 0.91 ± 0.11°C, and the 24‐h mean of rectal temperature 36.88 ± 0.22°C and 37.03 ± 0.14°C in the blind and the sighted subjects, respectively. These values between the two groups were not significantly different. The morning rise of rectal temperature began at ca. 3 a.m. in the sighted subject, but did not occur until at least 6 a.m. in the blind subject. The evening fall of rectal temperature also seemed to occur at later times in the blind subject. Our present findings suggest that the reduction of the ability to sense light and dark in the blind subject delays the phase of the rectal temperature rhythm, but it does not change the circadian pattern and the range of the oscillation in the rectal temperature rhythm. These findings are discussed from the viewpoint of circadian physiology.

Effects of cholecystokinin octapeptide on thermoregulatory responses and hypothalamic neuronal activity in the rat.

Rats were chronically implanted with a hypothalamic cannula to allow chemical stimulation of the hypothalamus on the conscious animals in repeated experiments. Direct administration of cholecystokinin octapeptide (CCK-8) (20-60 ng) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures of 8 degrees C and 22 degrees C. The hypothermia induced by CCK-8 was produced by a decrease in metabolism at an ambient temperature of 8 degrees C, whereas at 22 degrees C, it was caused by both a decrease in metabolism and an increase in cutaneous temperature. However, at an ambient temperature of 30 degrees C, intrahypothalamic administration of CCK-8 caused an insignificant change in thermoregulatory responses. Furthermore, neither intrahypothalamic injection of 0.9% saline nor intraperitoneal injection of CCK-8 (60 ng) had any effect on thermoregulatory responses at the ambient temperatures of 8 degrees-30 degrees C studied. Under urethane anaesthesia, 59 single neurons in the preoptic anterior hypothalamic area were examined in 29 rats. Each animal was subjected to scrotal warming or cooling and to the administration of CCK-8. Microiontophoretic application of CCK-8 resulted in inhibition of the majority (75%) of cold-responsive neurons as well as excitation of the majority (77.8%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (69%) of thermally unresponsive cells were not affected by CCK-8 application. The data indicate that CCK-8, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.