Adaptive timing of digestion and digestion-related thermogenesis in the pigeon

Pigeons were allowed to feed for 1 h either 2 h after lights on (morning pulse) or 3 h before lights off (evening pulse). Body temperature was measured radiotelemetrically. Faecal excretion, as an index of rate of digestion, was measured using load cells. At 22 degrees C, faecal excretion peaked just after lights-on in morning-pulse condition, but not in evening-pulse condition. In the cold (+5 degrees C), the peak was absent. We conclude that at thermoneutrality, pigeons are able to postpone a major part of digestion until late in the dark phase when their body temperature is increasing to the diurnal level. Thus, the extra heat from digestion-related thermogenesis that otherwise would be dissipated into the environment can be used for rewarming. In the cold, such a delay is not necessarily advantageous as the extra heat can always be used to substitute for thermoregulatory thermogenesis. The occurrence of concentrated period of digestion only in the morning-pulse condition was correlated to a lower food intake and lower body temperature as compared with the evening-pulse condition. Restricted feeding may thus be needed to induce adaptive timing of digestion as a mechanism of energy sparing. In addition to storage of food, timing of digestion may be a significant factor in the evolution of the crop in birds.     

Glutamate receptors in the raphe pallidus mediate brown adipose tissue thermogenesis evoked by activation of dorsomedial hypothalamic neurons

Disinhibition of DMH neurons with the GABAA receptor antagonist, bicuculline, increases heart rate (HR) and augments both brown adipose tissue sympathetic nerve activity (BAT SNA) and renal SNA (RSNA) contributing to the evoked increases in BAT thermogenesis and arterial pressure (AP). We determined the role of glutamate receptor activation in the rostral raphe pallidus (RPa) in mediating the sympathoexcitatory responses in HR, BAT SNA and RSNA following disinhibition of DMH neurons in urethane/chloralose anesthetized, artificially ventilated rats. Microinjections of either the selective NMDA receptor agonist, NMDA, or the selective non-NMDA receptor agonist, kainic acid (KA), into the RPa produced increases in BAT SNA (peak: + 502% and + 408% of control, respectively) and BAT temperature (peak: + 0.6 degrees C and + 1.0 degrees C) accompanied by rises in HR (peak: + 38 and + 63 bpm), RSNA (peak: + 57% and + 58% of control) and MAP (peak: + 12 and 15 mmHg). These responses were reversed by subsequent microinjection into RPa of the respective selective glutamate receptor antagonists, AP5 and CNQX. Microinjections of the non-selective glutamate receptor antagonist, kynurenic acid (Kyn), the NMDA receptor antagonist, AP5, or the non-NMDA receptor antagonist, CNQX, were effective in reversing the increases in BAT SNA (for Kyn, from peak of + 419% of control to + 9% of control) and BAT temperature, but not those in HR, MAP or RSNA (for Kyn, from peak of + 143% of control to + 124% of control) evoked by unilateral microinjection of bicuculline into the DMH. These results indicate that both NMDA and non-NMDA glutamate receptors in the RPa play a significant role in mediating the excitatory synaptic transmission producing the activation of BAT thermogenesis following disinhibition of DMH neurons. Glutamate receptors in the RPa may not be important for transmitting cardiovascular responses induced by activation of the DMH neurons.     

Thermoregulation and rheological properties of blood in primary Raynaud’s phenomenon and the vibration-induced white-finger syndrome

Objective: Frequent use of vibrating tools may lead to typical attacks of Raynauds phenomenon (RP). The present study assesses the feasibility of the use of thermographic measurements of blood rheometry in the diagnosis of vibration-induced white-finger (VWF) syndrome. Subjects and methods: We studied 38 patients that were suffering from RP (primary RP, n=29; VWF, n=9) and 13 controls (six men and 45 women; mean age 49.1±11.6 years). Superficial finger skin blood flow was assessed with an infrared thermocamera before and after exposure to heat and cold. Fibrinogen, whole-blood viscosity and erythrocyte aggregation at different shear rates and plasma viscosity were measured. Main results: In patients with RP finger temperatures after re-warming were lower than those in controls [right hand digit (DIG) I P<0.02; DIG II–V P<0.01; left hand DIG I P<0.01; DIG II-V p<0.02], male patients with primary RP had higher Fg-values (P<0.02) and a trend to higher plasma viscosity. Patients with VWF had a trend to lower plasma viscosity than controls. Whole-blood viscosity at each shear rate was highest in patients with VWF. Conclusion: Provocation manoeuvres are essential in the diagnosis of RP. We speculate that the decreased plasma viscosity in VWF is a compensatory physiological mechanism, probably counteracting the chronic effects of vasospasm. The rise in whole-blood viscosity could be due to endothelial injury or to a reduction in the venous blood pH level. The abnormal cold reactivity of patients with RP may be partly related to rheological factors.     

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.     

Restraint alters the thermic response to morphine by postural interference

The effects of morphine on body temperature have been shown to be altered by restraint. The purpose of this study was to determine how the type of restraint alters body temperature measurements and whether restraint alters the effects of morphine on body temperature by interfering with the ability of the rats to adjust their posture. The thermic effects of 5 doses of morphine (3.8 to 45 mg/kg) were compared in two types of restraint and confinement to a 13×20×20 cm pan without restrained, rats morphine caused predominantly hyperthermia, but with restraint morphine caused hyperthermia at low doses and hypothermia at higher doses. Morphine hypothermia was greater in rats restrained in rawire-mesh restrainer which prevented heat and humidity build-up than in the commonly used plastic restrainer. In the unrestrained rats, morphine treatment was associated with a posture characterized by exophthalamos, immobility, a hunched position and increased muscle tone. Restrained rats could not assume a compact posture. These results suggest that restraint alters the thermic effect of morphine and mainly by interferiing with postural mechanisms which reduce heat loss.     

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.     

Capsaicin pretreatment interferes with the thermoregulatory effect of morphine

Body temperature changes after the administration of 8 mg/kg morphine sulphate were studied in freely-moving and restrained rats, which were pretreated with capsaicin (300 mg/kg). Morphine caused a hyperthermic response irrespective of the previous capsaicin treatment in freely-moving rats; the lag time from the application of morphine to the hyperthermic maximum was, however, significantly delayed in capsaicin pretreated rats. A careful habituation to the experimental procedure (including injections, taking temperature, etc.) facilitated the hyperthermic response both in the pretreated and the control groups. Restrained rats typically showed a hypothermic response to the same dose of morphine. The drop of body temperature in habituated animals was significantly larger in the case of capsaicin pretreated rats. This potentiation of the hypothermic effect of morphine can be regarded as the primary site of interaction between capsaicin and morphine. Since capsaicin pretreated rats also showed an exaggerated thermoregulatory response to experimental stress, we conclude that the thermoregulatory effects of morphine and endogenous opiates are facilitated after capsaicin pretreatment.