Changes In Colonic Temperature Research Articles

Exposure to a maternal n-3 fatty acid-deficient diet during brain development provokes excessive hypothalamic–pituitary–adrenal axis responses to stress and behavioral indices of depression and anxiety in male rat offspring later in life

Brain docosahexaenoic acid (DHA, 22:6n-3) accumulates rapidly during brain development and is essential for normal neurological function. The aim of this study was to evaluate whether brain development was the critical period in which DHA deficiency leads to dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis in response to stress later in life. Rats were exposed to an n-3 fatty acid-deficient diet or the same diet supplemented with fish oil as an n-3 fatty acid-adequate diet either throughout the preweaning period from embryo to weaning at 3 weeks old or during the postweaning period from 3 to 10 weeks old. Exposure to the n-3 fatty acid-deficient diet during the preweaning period resulted, at weaning, in a significant decrease in hypothalamic DHA levels and a reduced male offspring body weight. DHA deficiency during the preweaning period significantly increased and prolonged restraint stress-induced changes in colonic temperature and serum corticosterone levels, caused a significant increase in GABAA antagonist-induced heart rate changes and enhanced depressive-like behavior in the forced swimming test and anxiety-like behavior in the plus-maze test in later life. These effects were not seen in male rats fed the n-3 fatty acid-deficient diet during the postweaning period. These results suggest that brain development is the critical period in which DHA deficiency leads to excessive HPA responses to stress and elevated behavioral indices of depression and anxiety in adulthood. We propose that these effects of hypothalamic DHA deficiency during brain development may involve a GABAA receptor-mediated mechanism.

Hypothermic retrograde jugular perfusion reduces brain damage in rats with heatstroke.

To determine whether direct retrograde ice saline infusion in the jugular vein without cardiopulmonary bypass protects rat brains after heatstroke. Randomized, controlled, prospective study. University physiology research laboratory. Sprague-Dawley rats (270-320 g, males). Rats were randomized into three groups and given a) no resuscitation after onset of heat stroke (HS, n = 8); b) ice saline infusion in the femoral vein after onset of heat stroke (HS + F, n = 8); or c) retrograde ice saline infusion in the external jugular vein after onset of heat stroke (HS + J, n = 8). Rats were exposed to an ambient temperature of 43 degrees C after vessel cannulation. Their mean arterial pressure, heart rate, colonic temperature, and brain temperature were continuously recorded. Survival time and brain pathology were checked. Although colonic temperature decreased 0.8-1.0 degrees C 15 mins after heatstroke in all groups, no treatment-related changes in colonic temperature were noted in any group. However, significant changes were observed in brain temperature. Fifteen minutes after heatstroke, brain temperature was 37.6 +/- 0.4 degrees C, 36.1 +/- 0.4 degrees C, and 33.6 +/- 0.8 degrees C in HS, HS + F, and HS + J, respectively. Survival time was 16.1 +/- 2.1, 33.0 +/- 3.8, and >120 mins in these groups, respectively. Neuron damage score was significantly lower in HS + J and without lateralization. We successfully demonstrated that direct retrograde hypothermic perfusion via the jugular vein without cardiopulmonary bypass protected the brain after heat stroke. This technique cooled the brain but did not significantly interfere with body temperature.

Role of L-type Ca 2+ channels in pertussis toxin induced antagonism of U50,488H analgesia and hypothermia

Previous studies have shown that the κ-opioid effects are sensitive to pertussis toxin (PTX) and affected by Ca 2+ fluxes. However, the possible involvement of Ca 2+ channels in PTX-induced inhibition of κ-opioid effects has not been reported. The effect of intracerebroventricular (i.c.v.) treatment of pertussis toxin (1 μg/rat, PTX) or saline on the κ-opioid agonist, U-50,488H (U5H) induced tail-flick analgesia and hypothermia in rats was determined. The effect of nimodipine (NIM), a dihydropyridine (DHP)-sensitive Ca 2+ channel blocker (CCB), on PTX-induced modulation of U5H effects was examined. The DHP ligand, [ 3H]PN200–110 binding was also determined in both PTX and saline treated rats to study the possible involvement of L-type Ca 2+ channels in PTX modulation of κ-opioid agonist effects. The analgesia and change in colonic temperature were determined using tail-flick analgesiometer and telethermometer, respectively. U5H (40 mg/kg, i.p.) produced significant analgesic and hypothermic responses. PTX treatment significantly ( P<0.01) antagonized the analgesic and hypothermic effects of U5H. Acute pretreatment of NIM (1 mg/kg, i.p.) 15 min prior significantly ( P<0.01) reversed the PTX-induced antagonism of U5H effects. In the binding study, PTX treatment (72 h before) resulted in a significant ( P<0.005) upregulation (+45% vs. saline control) of DHP binding ( B max) with no change in affinity ( K d). The results showed significant upregulation of DHP binding in accordance with PTX-induced antagonism of U5H effects and this blockade was reversed by NIM. Thus, present results suggest that U5H-induced analgesia and hypothermia may be mediated through PTX-sensitive transducer G-proteins (G i/o) coupled to L-type Ca 2+ channels.

Influence of Thyrotrophin‐Releasing Hormone on Thermoregulatory Adaptation after Birth in Near‐Term Lambs Delivered by Caesarean Section

We investigated the hypothesis that exogenous stimulation with thyrotrophin-releasing hormone (TRH) immediately prior to umbilical cord clamping can improve thermoregulatory adaptation after birth in near-term lambs delivered by Caesarean section. Lambs received an umbilical vein injection of saline +/- TRH (8 microg) prior to cord clamping. The rate of change in colonic temperature and oxygen consumption after birth were not influenced by TRH, but TRH-treated lambs exhibited a greater incidence of shivering compared with controls over the first hour of neonatal life. Two and a half hours after birth, TRH-treated lambs possessed brown adipose tissue (BAT) with a higher thermogenic activity (i.e. GDP binding to mitochondrial protein), but their BAT had a reduced DNA content and they had less hepatic glycogen than control lambs. TRH administration had no effect on iodothyronine 5' deiodinase activity in BAT and liver, or on plasma concentrations of total triiodothyronine, thyroxine, cortisol or free fatty acids. Three TRH-treated but no control lambs, failed to establish continuous breathing, so tissues from these treated lambs together with time-matched controls were sampled 25 min after birth. These 'non-surviving' TRH-treated lambs had very high plasma catecholamine concentrations, but their lung weights were similar to controls. 'Surviving' TRH-treated lambs possessed lungs with less DNA than non-surviving TRH-treated lambs. It is concluded that umbilical vein injection of TRH prior to umbilical cord clamping increases the recruitment of both shivering and non-shivering thermogenesis after birth.

EP1-receptor mediation of prostaglandin E2-induced hyperthermia in rats

To investigate what type of prostanoid receptors are involved in the development of fever induced by brain prostaglandin E2 (PGE2), PGE2 and its analogues were injected into a lateral cerebroventricle (LCV) of rats, and the changes in colonic temperature (Tco) were observed in a 23 +/- 1 degrees C environment. 17-Phenyl-omega-trinor-PGE2 (an EP1 agonist; 0.01-10 nmol) produced a rapid and dose-dependent rise in Tco. Even though the EP1 agonist was 10 times less potent than PGE2 on a molar basis, the time course of this hyperthermia was quite similar to that of the PGE2-induced one. No fever was elicited by an LCV injection of butaprost (an EP2 agonist; 0.1-100 nmol), 11-deoxy-PGE1 (an EP2 agonist; 0.1-1.0 nmol). The PGE2 (0.3 nmol)-induced hyperthermia was blocked by LCV pretreatment with SC-19220 (150 nmol), an EP1 antagonist. The results suggest that the PGE2-induced hyperthermia in the rat is mediated predominantly through EP1 receptors in the brain.

A spontaneous increase of salt intake and changes of colonic temperature in mice exposed to cold

The effect of repeated short-term exposure to cold on spontaneous salt (NaCl) intake and colonic temperature was investigated in two experiments on mice. In Experiment 1, half of a group of test animals were exposed to cold (7–9 °C; 6 h/day; 4 days), and half of both the exposed and non-exposed animals were allowed to choose between drinking water with (0.9%) and without (0%) NaCl. Food and fluids were provided all day long during the experiment. Mice provided with NaCl solution showed increased salt intake with cold exposure. Colonic temperature of mice was measured twice a day at the beginning and the end of cold exposure. Different changes in colonic temperature among the groups were observed at the end of cold exposure. In mice exposed to cold and provided with NaCl solution, colonic temperatures stayed unchanged, whereas in those without NaCl solution colonic temperatures decreased significantly after cold exposure. In Experiment 2, all the mice were exposed to cold as in Experiment 1. Four patterns of feeding of food and fluids were applied to groups of eight mice each: removal of food and fluids during cold; removal during 9 h before cold and during cold; removal during cold and during 9 h after cold, and feeding all day long. Half the mice in each feeding pattern were allowed to choose NaCl fluids (0% & 0.9%). Colonic temperature was measured as in Experiment 1. In all the feeding patterns, colonic temperature was significantly lower in the mice without NaCl solution than those with NaCl solution. Among four feeding patterns in mice with NaCl solution, colonic temperature was significantly higher in the case of feeding all day long than in the other three patterns.

Stereospecific effects of a κ-opiate antagonist on the actions of morphine in morphine-tolerant rats

The effects of κ-opiate receptor antagonist, MR 2266 and its dextro isomer, MR 2267 on morphine-induced analgesia and changes in colonic temperature were determined in morphine-naive and morphine-tolerant male Sprague-Dawley rats. Intraperitoneal administration of morphine (8 mg/kg) produced analgesia and hyperthermia in morphine-naive rats. MR 2266 (0.3-3.0 mg/kg) antagonized morphine-induced analgesia and hyperthermia in morphine-naive rats but MR 2267 was inactive. Subcutaneous implantation of six morphine pellets during a 7 day period induced tolerance to the analgesic and hyperthermic effects of morphine in the rat. MR 2266 also antagonized morphine analgesia and hyperthermia in morphine-tolerant rats, however, MR 2267 had no effect. A high dose (3 mg/kg) of MR 2266 produced an intense hypothermic response in morphine-tolerant rats. Previously we have shown that κ-opiate receptor agonists antagonize morphine analgesia in morphine-naive rats but potentiate it in morphine-tolerant rats. The results of the present studies indicate that the antagonist of κ-opiate receptors, on the other hand, antagonize morphine effects in both morphine-naive and morphine-tolerant rats in a stereospecific manner.

The binding of 3H-(3-MeHis 2)thyrotropin releasing hormone to brain membranes and temperature response to thyrotropin releasing hormone in different strains of mice

The effect of thyrotropin releasing hormone (TRH) on the colonic temperature of five strains of mice, namely, Swiss Webster, ICR, C57 BL, BALB and DBA, was determined. Intraperitoneal injection of TRH induced an hyperthermic response, the magnitude of which differed in different strains of mice. Peak effect was observed 15 min after the injection and the effect lasted for about an hour depending upon the dose. TRH produced a dose related hyperthermia in DBA mice, whereas in other strains an inverted U-shaped curve was obtained, with maximal response at 20 mg/kg and declining at 40 mg/kg dose. H-(3-MeHis 2) TRH bound specifically to brain membranes at a single high affinity site with a B max of 53.72 fmol/mg protein, and K d of 3.77 nM (for Swiss Webster mice). The K d and B max values did not differ for any strain. It Is concluded that the nature of TRH induced changes in colonic temperature depends both on the dose and the strain of mice, and that factors other than the brain receptors for TRH may be responsible for its variable hyperthermic effect.

Thermoregulatory and acute-phase responses to endotoxin of full- term-pregnant rabbits.

Fever, a fall in the plasma level of iron (Fe), and rises in the levels of certain plasma glycoproteins (indexed by protein-bound-N-acetylneuraminic acid [NANA]) normally occur during infection; they are thought to be mutually enhancing in host defense. It has been reported that fever is suppressed at full term of pregnancy; however, it is not known whether the blood chemical changes are similarly affected. Also, the mechanism for the suppression of fever is controversial. Since uteroplacental blood flow is at its maximum near term, competition between the demands of the fetoplacental unit and of thermoregulatory effectors might result in underperfusion of thermogenic tissues and therefore provide a basis for the lack of fever. To examine these questions, the changes in colonic temperature (Tco) and regional blood flow induced by Salmonella enteritidis endotoxin (LPS, 2 micrograms/kg iv) were compared in conscious nonpregnant and 30-day-pregnant rabbits 35 min after injection, using 15-microgram radiolabeled microspheres. In different rabbits, the effects of LPS on Tco and plasma Fe and NANA levels were measured before mating and at term. LPS induced fevers similar in heights and courses in both nonpregnant and full-term pregnant rabbits It caused decreases in the blood flows to brain, tongue, mammary gland, small intestine, and ear and increases in the blood flows to masseter muscle, bone, liver (hepatic artery), and left ventricle; blood flows to the kidneys, spleen, right ventricle, ovaries, and myometrium did not change. There were no significant differences in these vascular responses between nonpregnant and 30-day-pregnant rabbits, except a 28% reduction in the blood flow to the placentas.

Physiologic responses to chronic dietary tyrosine supplementation in DOCA-salt-treated rats.

The antihypertensive effect of chronic administration of L-tyrosine (Tyr) was investigated in a two-part study. In the first experiment, adult male Sprague-Dawley rats were assigned to 1 of 4 treatment groups: control diet plus unilateral nephrectomy (Nphx) and 0.15 M NaCl (Sal) as the sole drinking solution (C-CTRL); control diet plus deoxycorticosterone acetate (DOCA, 268 micrograms/rat/day), Nphx, and Sal (C-DOCA); control diet supplemented with 2.5% L-p-Tyr plus Nphx and Sal (Tyr-CTRL), and Tyr plus DOCA, Nphx, and Sal (Tyr-DOCA). Systolic blood pressure (SBP) increased within 2 weeks after initiation of treatment with DOCA-salt and remained elevated throughout the duration (8 weeks) of the study (p less than 0.001). Dietary administration of Tyr to DOCA-treated rats failed either to affect SBP in normotensive rats or the elevation of SBP in DOCA-treated rats. Dietary supplementation with Tyr induced a significant elevation in urinary excretion of free dopamine (week 1, 3, 5, and 7) and a decreased excretion of free norepinephrine (week 1) without regard to DOCA treatment. Metabolic responsiveness (change in colonic temperature) and cardiovascular responsiveness (change in heart rate) to subcutaneous administration of the beta-adrenergic agonist, isoproterenol, were significantly prolonged while alpha 2-adrenoceptor number (cerebral cortical membranes; 3H-yohimbine binding) was reduced in rats receiving Tyr. In the second experiment, similar rats were assigned to 1 of 3 treatment groups: control diet plus Nphx and Sal, control diet plus Nphx, DOCA and Sal, and Tyr plus DOCA, Nphx, and Sal; however, Tyr was not started until DOCA-salt-induced hypertension developed (4 weeks). Neither acute (2.5 h post-meal) nor chronic (4 weeks) effects of administration of Tyr on SBP were noted. Thus, the Tyr-induced changes observed in these studies include a chronic increase in free dopamine, and a transient decrease in norepinephrine, excretion. No significant effects of Tyr on blood pressure of DOCA-salt-treated rats were observed.

Heart rate changes due to 5.6-GHz radiofrequency radiation: relation to average power density.

Effects of intermittent exposure to 5.6-GHz radiofrequency radiation (RFR) on heart rate, blood pressure, and respiratory rate were examined in anesthetized rats. During exposure to 60 mW/cm2 which resulted in a 1 degree C change in colonic temperature, heart rate increased; the values returned to control levels after exposure was discontinued. No changes in mean arterial blood pressure or in respiratory rate were observed. Exposure to 30 mW/cm2 caused no significant changes in heart rate, blood pressure, or respiratory rate. The data indicate that heart rate changes during exposure to 5.6-GHz RFR are related to the average power density applied, and thus to the rate of change in temperature, and not simply to the absolute change in temperature.

Absence of endotoxin fever but not prostaglandin E2 fever in the Brattleboro rat.

Changes in colonic temperature following intracerebroventricular injection (icv) of bacterial endotoxin or prostaglandin E2 (PGE2) were measured in Long-Evans (LE) and Brattleboro (DI) rats. Indwelling cannulas were implanted into the brains of rats for subsequent microinjection into a lateral cerebral ventricle. Microinjection of 1 microgram of bacterial endotoxin into a lateral cerebral ventricle produced a fever in the LE rat but not in the DI rat. Daily injections of 1 microgram of endotoxin icv in the DI rat did not result in a fever. Intraperitoneal injections of 50 micrograms of bacterial endotoxin resulted in a fever in the LE rat, but the DI rat showed no such response. Both groups of animals did produce a fever in response to icv administration of 200 ng of PGE2. The lack of arginine vasopressin in the DI rat may be related to the animal's failure to show a febrile response to endotoxin.

Thermoregulatory characteristics of neurogenic hyperthermia in the rat.

1. The thermoregulatory characteristics of the neurogenic hyperthermia produced in rats by unilateral mechanical destruction of the rostral hypothalamic/preoptic region were studied. 2. The investigational methods employed included (a) observing the thermoregulatory effector activities which were responsible for generation of hyperthermia, (b) observing the thermoregulatory reactions elicited by forcefully elevating or lowering core temperature during neurogenic hyperthermia and (c) observing the effect of ambient temperature on hyperthermia magnitude. 3. At 26 degrees C, hyperthermia was effected by a transient increase in shivering thermogenesis and a concomitant minimization of heat loss through the tail. 4. At 26 degrees C, perturbations of core temperature during the plateau phase of hyperthermia were induced by internal or external heating and cooling. The disturbances elicited compensatory changes in shivering activity and in tail vasomotor tonus, and core temperature was rapidly and precisely returned to its pre-perturbation level. 5. The magnitudes of hyperthermias experienced by rats lesioned at 10, 15, 26 and 32 degrees C, as measured by the change in colonic temperature and by the area under the fever curve, were not significantly different. At 36 degrees C, rats were hyperthermic prior to lesioning, and the magnitude of the lesion-induced hyperthermia was significantly attenuated. 6. The results indicate that the neurogenic hyperthermia produced by unilateral hypothalamic puncture in the rat is generated by a coordinated modulation of thermogenic and heat retentive effectors and that the plateau level of hyperthermia is well regulated. These characteristics are compatible with the hypothesis that neurogenic hyperthermia is mediated by prostaglandins released from injured tissue and acting on surviving rostral hypothalamic tissue.

Neurotensin and bombesin: differential effects on body temperature of mice after intracisternal administration

Intracisternal administration of neurotensin or bombesin produces a significant hypothermic response in rodents in an ambient temperature of 23°C or below; bombesin has been reported to produce a significant hyperthermic response in rats at 36°C, but no change in colonic temperature at ambient temperatures between 31 and 33°C. In this study we compared the effects of the two neuropeptides on colonic temperature of mice exposed to different ambient temperatures to determine whether neurotensin also produces a poikilothermic state. From a series of experiments conducted at ambient temperatures of 4, 23, 26, 30, 34 and 38°C, in which mice received an intracisternal injection of an equimolar dose (0.6 nmol) of neurotensin or bombesin (or vehicle), we noted that the two neuropeptides produce different effects on colonic temperature. At ambient temperatures of 26°C and below, both neurotensin and bombesin produce a significant hypothermic response; however, at higher temperatures bombesin has no effect (30°C) or produces hyperthermia (34°C). In contrast, neurotensin produces hypothermia at 30°C and no significant effect at 34 and 38°C. In addition, a wide range of doses of neurotensin failed to produce the poikilothermic effects characteristic of centrally administered bombesin.

Effects of tracheal bypass breathing on heat balance in rabbits.

The effects of obstruction of the air passage through the nose on hypothalamic temperature (Thy) and heat balance were studied in 37 conscious rabbits using a direct calorimeter. The obstruction of the air passage through the nose was made by forcing the animal to breathe through a tracheal bypass cannula at a calorimeter wall temperature (TW) of either 17, 22, 26, or 28 degrees C. By bypass breathing, Thy and sensible heat loss (HL dry) were increased without a significant change in colonic temperature in a warm environment. At TW 28 degrees C, Thy in bypass breathing was 39.52 +/- 0.13 degrees C while that in nose breathing was 39.30 +/- 0.11 degrees C (p less than 0.05). HL dry in bypass breathing was 29.3 +/- 0.8 W . m-2 while that in nose breathing was 24.8 +/- 0.6 W . m-2 (p < 0.01). However, evaporative heat loss (Hl wet) was not changed by bypass breathing, although the respiratory rate was increased slightly. These results indicate that the obstruction of air passing through the nose increases hypothalamic temperature and elicits a thermolytic response only through the increase in sensible heat loss in the TW 28 degrees C environment. Heat production (M) was not suppressed by bypass breathing at TW 28 degrees C, at which the value of M was already minimum (42.0 +/- 3.0 W . m-2). In the 17-26 degrees C range of TW, heat balance was roughly obtained in either nose or bypass breathing. At TW 28 degrees C, however, M was slightly higher than HL, and a positive shift of heat storage was assumed particularly in nose breathing.

Serotonergic influences on brain stem thermoregulatory mechanisms in the cat

Summary To investigate the pharmacological and functional characteristics and anatomical locations of putative serotonergic synapses in the brain stem thermoregulatory pathways of the cat, 0.01-0.03 M 5-hydroxytryptamine (5-HT) was injected through chronically implanted guide cannulae into 160 cerebral loci in 15 cats. 5-HT injected at 115 sites caused no immediate change in colonic temperature. Injections into 19 sites within the rostral portion of the hypothalamus produced shivering and an immediate, short-lasting hyperthermia. Injections into 26 sites within the preoptic/basal forebrain region produced peripheral vasodilation and an immediate, short-lasting hypothermia. Both types of immediate effect were dose-dependent, susceptible to blockade by methysergide administered systemically or into the 5-HT injection site, and resistant to indomethacin pretreatment (10 mg/kg i.p.), and both were often followed by a long-lasting hyperthermia which could also be elicited by injections of control solutions. The delayed hyperthermia produced by 5-HT injections into rostral hypothalamic loci was strongly attenuated by indomethacin pretreatment, an indication that the effect was mediated by the release of pyrogenic prostaglandins. It can be concluded that the sole pharmacologically specific effects of the 5-HT injections were the short latency, transient hyperthermic and hypothermic episodes. These results suggest that serotonergic synapses in the rostral and caudal aspects of the classical ‘preoptic/anterior hypothalamic region’ mediate functionally opposing thermoregulatory effects, those in the rostral aspect being involved in heat dissipation and those in the caudal aspect, in heat gain. The implications of these findings with respect to existing neurochemical models of thermoregulation are discussed.

Improved cold tolerance and its mechanism in cold-acclimated rats by high fat diet feeding.

Cold tolerance and metabolic responses to cold were studied in cold-acclimated rats on high fat diet (CAHF). Cold tolerance at-5 degrees C was assessed by fall of colonic temperature of clipped rats after 18 h of fasting. Rate of fall in colonic temperature was greatest in warm-acclimated control rats (WAST), slowest in cold-acclimated rats on standard diet (CAST), and remained unchanged in CAHF during cold exposure for 240 min. Increment in blood free fatty acid (FFA) concentration 80 min after cold exposure was greatest in WAST, less in CAST, and least in CAHF. Blood glucose decreased similarly in WAST and CAST after cold exposure, while it remained unchanged in CAHF. Blood beta-hydroxybutyrate also increased similarly in WAST and CAST, while it did not change in CAHF. Nonshivering thermogenesis tested by noradrenaline was greatest in CAHF, followed by CAST and WAST. Shivering induced by cold exposure was less pronounced in CAST than in WAST and did not develop in CAHF; changes in colonic temperature were inversely related to the extent of shivering during cold exposure for 90 min. These results suggest that an integrating effect of cold and high fat diet could improve cold tolerance much more than cold acclimation itself, possibly through enhanced nonshivering thermogenesis caused by metabolic modifications such as increased lipid use and gluconeogenesis.

The effects of D-amphetamine and related drugs on colonic temperatures of rats kept at various ambient temperatures

The effects of D-amphetamine on the colonic temperature of the rat vary markedly with the ambient temperature. At fixed relative humidities, D-amphetamine causes a dose-dependent hyperthermia among animals placed in warm environments (20–37°C), and hypothermia among rats placed in the cold (4–15°C). The changes in colonic temperature that follow the administration of chlorpromazine, reserpine, tyramine, fenfluramine, or pimozide also depend upon the ambient temperature. Since tyramine treatment mimics the hyperthermic, but not the hypothermic, effects of D-amphetamine, and since D-amphetamine-induced hypothermia is blocked by pimozide, this hypothermia may involve central dopaminergic neurons.

The role of hypothalamic temperature in the control of panting in the chicken exposed to heat.

1. In unanaesthetized chickens, the temperatures of the hypothalamus, colon and skin have been recorded in relation to the onset and cessation of thermally induced panting.2. During control conditions, hypothalamic temperature showed fluctuations associated with arousal and movement. It was lower than colonic temperature by about 0.9 degrees C but this difference generally decreased during exposure to heat.3. When the birds were exposed abruptly to 40 degrees C, or to ambient temperatures increasing gradually from 20 to 52 degrees C, there was a delay of 15-65 min and marked increases in both peripheral and central body temperatures before panting commenced.4. Infra-red irradiation of the thorax and abdomen caused vasodilatation in the comb and toe before detectable increases in the deep body temperatures. Increasing the colonic temperature by up to 2 degrees C did not cause panting until hypothalamic temperature was also raised. This inhibitory effect of normal hypothalamic temperature was enhanced by low ambient temperature.5. Infra-red irradiation of the head increased hypothalamic temperature by up to 3.5 degrees C and caused vasodilatation in the toe without changes in colonic temperature. Panting, however, did not occur so long as colonic temperature was within the normal range. The inhibitory effect of normal colonic temperature was again enhanced by low ambient temperature.6. In anaesthetized chickens, selective heating of the head and body caused panting only after increases in both the hypothalamic and colonic temperatures.7. Repeated exposure of birds to 40 degrees C did not reduce the time delay before panting started.8. It is concluded that panting in the fowl requires an increase in some extracranial deep body temperature as well as in that of the hypothalamus.

The acute rectal toxicity of acetylsalicylic acid.

The LD50 ± S.E. of acetylsalicylic acid administered rectally to male albino rats was found to be 0.79 ± 0.027 g/kg, which is significantly less than the oral LD50. The minimal dose producing toxic symptoms was about 0.20 g/kg. The most significant toxic signs were ataxia, drowsiness, dyspnea, pallor, diarrhea, and anorexia. The immediate cause of death was respiratory failure preceded by coma or clonic convulsions. Loss in body weight, inhibition of food intake, and interval until death were dose-dependent. The drug caused diuresis and aciduria but no significant changes in colonic temperature, or in urinary glucose or protein. Death at 4 to 9 hours was associated with extensive capillary–venous congestion and at 24 hours and over with degenerative changes in the kidneys and liver. Congestive and hemorrhagic ulcers appeared in the pyloric stomach at 4 hours, reached a peak at 24 hours, and thereafter began to heal. Local reaction in the colon and cecum was limited to mild inflammation. Significant loss of weight and a gain in water level occurred in most organs.