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Serum free fatty acid level and body temperature changes in emotional stress in rabbits. Effect of hydroxydial.

Fourteen New Zealand rabbits were immobilized for 75 minutes During this time the ear (Te) and rectal (Tre) temperatures were measured at 5 min intervals. Immediately before immobilization, and then in the 35th, 55th, and 75th min of immobilization blood samples were taken for determinations of the serum free fatty acid (FFA) levels. A statistically significant fall of Tre and a significant rise in the serum FFA levels were observed at the end of immobilization. The ear temperature in these animals exceeded considerably the values as normal. Intravenous administration of hydroxydial 0.1 mg/kg before repeated immobilization prevented body temperature changes and blood FFA level rise in half the animals. In the remaining animals the changes became more intensive. It is supposed that the tested rabbits differed in their reactivity to stressful stimuli, and this hypothesis was confirmed by experiments in which weaker stimuli were used. Repetition of stressful stimuli increased the intensity of these autonomic responses in all animals.

Animals↗

Changes in body temperature after administration of amino acids, peptides, dopamine, neuroleptics and related agents.

Drugs may alter body temperature by acting on any component of the thermoregulatory system. These components include heat production, heat conservation and heat loss effectors and their efferent pathways, thermosensors and their afferent pathways and neurons within the central nervous system that coordinate thermoregulatory effector activities. A thermostat is often thought to be involved although thermoregulation can be explained by models that do not incorporate a thermostat. An action on a particular component can be assessed by determining the effect of a drug on body temperature over a range of environmental temperatures and by observation and measurement of associated changes in effector activities. A scheme for such assessment is presented along with examples of its use. The study of drug-induced changes in body temperature has expanded greatly within the past decade. The primary purpose of this review is to provide a readily available source of information on interactions between certain drugs and the thermoregulatory system. Extensive tables are presented of body temperature changes after administration of amino acids, peptides, dopamine and related agents, phenothiazine neuroleptics and also phenothiazines that lack neuroleptic activity, butyrophenones, diphenylbutylpiperidines such as pimozide and miscellaneous neuroleptics. The information tabulated includes the species used, route of administration and dose of drugs, the environmental temperature at which the experiments were performed, the number of tests, the direction and magnitude of body temperature change and remarks on the presence of special conditions, such as age or lesions, or on the influence of other drugs, such as antagonists, on the response to the primary drug. Most of the cited literature was published since 1965.

Amino Acids↗

Intracellular pH in cold-blooded vertebrates as a function of body temperature.

Intracellular pH (pHi) was measured in vivo in tissue of frogs (Rana catesbeiana) and turtles (Pseudemys scripta) using the DMO technique. Animals were permitted 3-8 days to come to a new steady-state body temperature (Tb) which ranged 5-32 degrees C. Least squares regression equation for pHi data are: frog blood, 8.184-0.0206 Tb; frog striated muscle, 7.275-0.0152 Tb; turtle blood, 8.092-0.0207Tb; turtle muscle, 7.421-0.0186 Tb; turtle heart, 7.452-0.0122 Tb; turtle liver, 7.753-0.0233 Tb; turtle esophageal smooth muscle, 7.513-0.0141 Tb. Only turtle cardiac muscle deltapHi/deltaT was significantly different from deltapH/deltaT of blood. Results have been interpreted in terms of protein charge state alterations; in the physiological pH range, histidine residues of proteins are the principal dissociable groups (HPr+ = H+ + Pr) affected by pHi and Tb changes. Constancy of protein charge state can be assessed by monitoring alpha imidazole, alphaIM = Pr/(HPr+ + Pr). A uniform pKIM of 6.85 (20degreesC) and a deltaHO of 7 kcal/mol are assumed in calculating alphaIM. Intracellular alphaIM is preserved in the tissues studied as body temperature changes. These results indicate that ectotherm acid-base balance, alphastat control, regulates not only extracellular blood proteins, but also intracellular compartment proteins in such a way as to preserve functions dependent upon protein net charge states.

Acid-Base Equilibrium↗

Transcriptome analysis of brown adipose tissue in Brandt's vole treated with tannic acid under cold exposure.

BACKGROUND: Tannic acid (TA) is a hydrolysable plant secondary metabolite known to influence multiple physiological processes in animals; however, its role in regulating brown adipose tissue (BAT) thermogenesis remains poorly understood. Notably, the overwinter food caches of Brandt's voles predominantly consist of Artemisia species, which are rich in TA. This study aimed to determine whether TA contributes to cold tolerance in Brandt's voles by activating BAT thermogenesis. Adult male voles were administered TA, after which the masses of BAT and inguinal white adipose tissue (iWAT) were measured, and temperature changes in BAT, the body surface, and the rectum were recorded following exposure to - 20 °C. In addition, transcriptomic analyses of BAT were performed, and the expression and protein levels of key thermogenic markers were assessed. RESULTS: The results showed that TA reduced iWAT mass while exerting minimal effects on BAT mass. TA-treated voles exhibited significantly elevated temperatures in BAT, the body surface, and the rectum after cold exposure. Histological analyses revealed that TA treatment reduced adipocyte area in iWAT while increasing the number of nuclei in brown adipocytes in BAT. In BAT, differentially expressed genes (DEGs) in voles receiving a low TA dose were significantly enriched in pathways related to fat digestion and absorption and peroxisome proliferator-activated receptor (PPAR) signaling. In contrast, DEGs in voles administered a high TA dose were predominantly associated with brown adipocyte differentiation and the upregulation of cold-induced thermogenesis. Moreover, TA administration increased the expression of FFAR4 and UCP1, as well as the protein levels of PGC-1α, PPARγ, and UCP1 following cold exposure. CONCLUSIONS: Collectively, these findings demonstrate that TA enhances cold tolerance in Brandt's voles by promoting thermogenic gene expression and stimulating brown adipocyte differentiation in BAT, providing novel insights into the role of plant secondary metabolites in mammalian cold adaptation and herbivore-plant interactions.

Animals↗

Sodium regulation in the larvae of Chironomus dorsalis (Meig.) and Camptochironomus tentans (Fabr.): the effect of slat depletion and some observations on temperature changes.

Sodium regulation was studied in fourth instar larvae of Chironomus dorsalis and Camptochironomus tentans. Both maintain a body sodium level well above that of the surrounding medium. The haemolymph contains approximately 90% of total body sodium and approximates to a single compartment freely exchanging sodium with the external medium. The anal papillae play a primary role in sodium regulation, the gut being in secondary importance. Sodium regulation in both species is comparatively insensitive to alterations in acclimatization temperature. C. dorsalis and C. tentans are capable of maintaining sodium balance in media containing 10 mumole Na and 25 mumole Na respectively. When exposed to several changes of distilled water, C. tentansis capable of reducing sodium loss by elaboration of a more dilute urine. This is apparently,supplemented by a reduction in the permeability of the body surface. Activation of sodium uptake in both species is comparatively sluggish, with influx reaching a maximum only after the loss of greater than 30% body sodium.

Animals↗

Hypothalamic heating and cooling in monoamine-depleted rabbits.

The role of monoamines in the thermoregulatory responses induced by hypothalamic heating and cooling was investigated in conscious rabbits. Depletion of hypothalamic catecholamines by pretreatment with 6-hydroxydopamine (6-OHDA) greatly attenuated the rectal temperature and vasomotor responses to hypothalamic heating and cooling. Pretreatment with p-chlorophenylalanine (PCPA) depleted the animals of 5-hydroxytryptamine (5-HT). The results obtained are consistent with 5-HT having an inhibitory role in the rabbit's vasomotor response to heat stress and activating heat conservation during cold stress. Reserpinized rabbit were depleted of both norepinephrine (NE) and 5-HT and were found to be unresponsive to hypothalamic temperature changes. We conclude that the integrity of the monoaminergic system is viral for the correct functioning of the hypothalamus in maintaining a constant body temperature.

Animals↗

Effects of temperature transients on gas exchange and acid-base status of turtles.

Pulmonary ventilation (VE), O2 consumption (VO2), and CO2 production (VCO2) were measured continuously on each of 10 turtles, Pseudemys scripta elegans, at 20 degrees C, during and for 1 h after heating to 30 degrees C and during and for 1 h after cooling to 20 degrees C. In seven of the animals, arterial blood was sampled at the three temperature plateaus. Ventilatory ratios (VE/VO2 and VE/VCO2) and metabolic rate adjusted promptly to temperature change, stabilizing at values similar to those observed previously in turtles following 1 day or more at each temperature. Likewise, mean blood pH and PCO2 values conformed both in absolute values and in temperature-dependence to data previously obtained from animals exposed to the various temperatures for longer time periods or from turtle blood thermally equilibrated in vitro. Total plasma [CO2] did not change significantly, suggesting that steady-state CO2 exchange prevailed throughout the experiment. In accordance with this, R(VCO2/VO2) did not change significantly during the 20-30 degrees C transition; however, R rose during the 30-20 degrees C transition, suggesting possible hyperventilation at this stage. We conclude that the respiratory control of blood acid-base status adjusts rapidly to temperature change in the turtle and its adjustment minimizes disturbance to CO2 balance.

Acid-Base Equilibrium↗

Thermography and rheumatic diseases.

The common factor in most of the rheumatic diseases is an arthritis. Radiometry and thermography have been shown to indicate and measure heat resulting from localised inflammation. In rheumatoid arthritis, juvenile arthritis, osteoarthrosis, gout and ankylosing spondylitis abnormal heat distribution has been recorded over affected joints. Experimental evidence has shown that temperature change reflects the inflammatory state of the joint, and that this may be used to measure the effect of therapy by oral, systemic and local drug therapy, and also surgery, i.e. synovectomy.

Adrenocorticotropic Hormone↗

Warm receptors in the dorsal abdominal wall of the rabbit.

Warm stimulation of a circumscribed region of the dorsal abdominal wall of the rabbit evoked discharges in splanchnic afferent single fibers. They showed positive temperature coefficients of their static activities and of their dynamic responses to temperature changes. They were not excited by mechanical stimuli. Cooling from static conditions caused a transient inhibition of impulse frequency. Two populations were found, one having a static and dynamic maximum at 46 degrees C, the other one at about 40 degrees C. Both types were found to be C-fibers, with a conduction velocity of 0.6 - 1.1 m/sec.

Abdominal Muscles↗

Types of neuronal responses in the rat thalamus to peripheral temperature changes.

Recordings were made of spike-trains from 163 neurons of the rostral part of the ventrobasal thalamus complex of the rat while the temperature of the scrotal skin was altered. The following results were obtained: 55 neurons were non-thermosensitive, 7 neurons cold-sensitive and 101 neurons warm-sensitive. In the case of the warm-sensitive cells a definite discrimination was possible: 61.4% of the neurons altered their firing behavior during peripheral cooling, changing from relatively even spike frequency to burst firing. This change could be induced repeatedly by altering the temperature. 38.6% of the neurons, on the other hand, reacted to cooling by slowing down their frequency. By way of statistical methods the firing patterns of the two response-types were analyzed more precisely and the differences in response to temperature stimuli more exactly defined. Likewise, the spatial distribution of the two response-types of warm-sensitive cells exhibited differences; whereas the cells devoid of burst activity occured rather uniformly in the region of the thalamus studied, the cells with bursting activity were confined more to the mediocaudal region. These findings are discussed with regard to the phenomenon of peripheral bursts and to the projection of thermoafferent pathways onto the ventrobasal thalamus complex. The functional interpretation of the various cell reactions and their role in the central processing of thermoafferent signals still remains unexplained and requires comparative studies of peripheral and central parts of the thermoafferent system.

Animals↗

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.

Animals↗

Intracellular acid-base state at a variable temperature in air-breathing vertebrates and its representation.

When temperature changes are superimposed on changes in the control variables of acid-base state (PCO2, strong ion difference), the understanding of acid-base changes becomes difficult. A solution has recently been proposed for blood (Malan, 1977); it was based on the assumption that closed system conditions correspond to a minimal change in the overall acid-base state when temperature varies. The feasibility of extending these concepts to muscle intracellular acid-base vs temperature relationships is evaluated on the basis of a model study; the errors made by replacing closed conditions (which require knowledge of chemical composition) by more convenient approximations are estimated. A representation of both extracellular and intracellular acid-base data on a temperature-corrected bicarbonate-pH diagram is derived. It allows the interpretation of variable-temperature intracellular acid-base changes in terms of changes in control variables, 'respiratory (PCO2) or 'metabolic' (strong ion difference).

Acid-Base Equilibrium↗

Dependence in rats after one injection of heroin-, LAAM- or hydromorphone-zinc tannate.

Complex zinc tannate salts of heroin, hydromorphone and l-alpha-acetylmethadol were synthesized and injected in a slow-release vehicle, into rats. One, 3, 7, 10 and 14 days after the drug was administered rats were injected with naloxone hydrochloride (10 mg/kg) and during the following 4 hours body weights, core temperature and behavioral signs such as diarrhea, writhing, teeth chattering and wet dog shakes were recorded. On every naloxone testing day the narcotic-treated groups presented behavioral signs of abstinence, but weight loss and temperature changes were much less consistent. Reduction of core temperature following naloxone administration seems to be an earlier indicator of physical dependence than weight loss. According to the parameters tested a level of physical dependence can persist for at least two weeks after a single injection of these narcotic salts.

Animals↗

The initial heat production in garfish olfactory nerve fibres.

A study has been made of the temperature changes associated with the passage of a single impulse in the non-myelinated fibres of the garfish olfactory nerve: and the time course of these temperature changes has been compared with the time course of the electrical events during the action potential. As in other non-myelinated nerves studied the observed temperature changes result from a biphasic initial heat production consisting of a transient evolution of heat (the positive heat) followed by a rapid heat reabsorption (referred to as the negative heat). There is no evidence of any additional phases of initial heat production. At 0 degrees C the measured positive initial heat is 224 mucal/g impulse (937 muJ/g impulse); and the corresponding negative initial heat is 230 mucal/g impulse (962 muJ/g impulse). The residual initial heat is very small, being about -6 mucal/g impulse (-25 muJ/g impulse). In the range 0-10 degrees C there is no significant effect of temperature on the magnitude of either the positive or the negative phases of heat production. The experimental thermal records were analysed to determine the true time course of the temperature changes in the nerve undistorted by the recording system. The time course of the temperature changes does not fit with that of the transmembrane voltage change as represented by the monophasic compound action potential recorded externally from the same point on the nerve. A better fit is obtained if the temperature changes are compared with the square of the voltage change in accordance with the view that the heat derives almost wholly from free energy changes and entropy changes in the membrane capacity. The best fit is obtained if it is assumed that the membrane potential does not discharge to zero during the action potential but that at the peak of the action potential the charge (and hence the p.d.) across the membrane capacity retains about 24% of its resting value.

Action Potentials↗

A comparative study in Porcellio laevis (Lat.) and Armadillidium vulgare (Lat.): response to temperature, photoperiod and oxygen concentration.

Relationship of body weight, imposed fasting, temperature, light intensity, and oxygen concentration to oxygen consumption in Porcellio laevis and Armadillidium vulgare has been investigated in a series of laboratory experiments. It was observed that (1) the metabolic response in the two species to temperature change was a uniform increase of oxygen consumption with increasing temperature from 15 degrees C to 60 degrees C. Beyond 30 degrees C, the oxygen consumption in each species fell, and the thermal death point was reached at about 40 degrees C. (2) The response to decreasing oxygen concentrations was a corresponding decrease in oxygen consumption. Armadillidium vulgare was a partial regulator while Porcellio laevis was able to conform its internal state to the changing oxygen levels. (3) In each species there was a decrease in metabolic rate with increasing body weight. (4) On the basis of their general activity level and oxygen consumption rate, Porcellio appeared to be a nocturnal species, while Armadillidium had a day active metabolism.

Animals↗

Endotoxin fever in the newborn kitten. The role of prostaglandins and monoamines.

In 5--10 day-old kittens at thermoneutral environmental temperature cerebroventricular injections of 10 microgram serotonin or noradrenaline caused hyperthermia and hypothermia, respectively. Central injections of 20 and 200 ng prostaglandin E1 induced hyperthermia. Monophasic fever followed the cerebroventricular injections of 0.2 or 0.002 microgram E. coli endotoxin, both in thermoneutral and moderately cool environments. In kittens pretreated with para-chlorophenylalanine (PCPA) the endotoxin induced rise in body temperature was attenuated within 60 to 90 min after the endotoxin. Indomethacin pretreatment prevented the first part of the febrile response and only a slight temperature rise occurred after a long latency. Central injections of phentolamine did not modify the fever response, while centrally applied propranolol modified the fever course so that it resembled that seen in PCPA treated kittens. The central mediation of endotoxin fever in the kitten is complex, despite that the pattern of the temperature change is simple (monophasic). Arachidonic acid metabolites and serotonin of the central nervous system may be involved in the reaction, while the activation of central noradrenergic mechanisms does not seem to be indispensable for the response. The changes in mediators are similar to those in newborn guinea pigs, although the fever course is different in the two species.

Animals↗