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PubMed1979

Measurement of heat production in dog submandibular gland.

In dog submandibular glands, we measured changes in metabolic heat production during a secretory period which was induced by electrical stimulation of the chorda tympani. When measured with fine thermocouples, the temperature of both the gland itself and venous blood from the gland increased by 0.1-0.7 degrees C at the maximum. The blood flow was about 0.3 g.min-1.g-1 wet weight of gland at a resting period and increased to 1-3 g.min-1.g-1 at the maximum of secretory response. The resting heat production in vitro, measured by a microcalorimeter, was 3.3 mW.g-1 at 27 degrees C and 7.8 mW-g-1 at 37 degrees C. The specific heat of the blood and the salivary gland, measured by a microcalorimeter, were 3.97 and 3.91 J.g-1, degrees C-1, respectively. The change in conductive heat loss, measured by a thermopile under stimulated conditions, ranged from 4 to 6 mW.g-1 at the maximum. Metabolic heat production during secretion in vivo (37 degrees C) was estimated from temperature changes in the glandular tissue and blood, blood flow, specific heat and resting heat production. Values obtained were in the range from 15 to 80 mW.g-1 at the maximum. Heat production increased rapidly within the first 20 sec to reach a maximum and then declined with time, but slow heat production continued. On the basis of the present results together with those from former studies on ionic transport in the salivary gland, we discussed the relation of heat production to transport of substances during secretory processes.

Animals↗

PubMed1979

Graded changes in central chemoceptor input by local temperature changes on the ventral surface of medulla.

1. In cats under pentobarbitone anaesthesia the effects of focal temperature changes of the ;chemoceptive' areas on the ventral surface of medulla, described by Loeschcke and his associates, were studied with respect to tidal volume, V(T), tidal variation in efferent phrenic activity, Phr(T), and respiratory rate. The cats were either paralysed and ventilated at various constant P(A,CO2) and P(a,O2) levels, or breathing spontaneously.2. It was confirmed that focal bilateral cooling of the intermediate, ;I((S))', areas caused rapid depression of respiration even at constant artificial ventilation. In normocapnic and normoxic conditions apnoea usually ensued at brain surface temperatures of 20-22 degrees C.3. The effects were graded along continuous temperature-response curves with enhancements of ventilation above and depression below normal body temperature.4. The strongest effects on V(T) and Phr(T) were obtained from the I((S)) areas with no or only small effects on inspiratory or expiratory timing in the vagotomized animal. The Hering-Breuer inflation reflex and its effects on timing and amplitudes were not affected by cooling this area.5. Focal cooling of the caudal or the rostral ;chemoceptive' areas, ;C((L))' and ;R((M))' areas, caused smaller effects on V(T) and Phr(T) but produced significant effects on respiratory rate even after vagotomy.6. The effects of focal cooling of these areas could be mimicked by topical application of procaine solution which has been shown not to penetrate deeper than 100 mum from the surface.7. Moderate focal cooling of area I((S)) to temperatures above 28-30 degrees C caused a parallel shift in the CO(2)-response (V(T), Phr(T)) curves to the right with little change in slope. The P(CO2) thresholds for apnoea were correspondingly raised. These focal temperature effects could be compensated by changes in P(CO2) with, on the average, 2.7 torr/ degrees C. Focal temperatures below 28 degrees C usually caused some decrease in slope of the CO(2)-response curves in addition to further shifts.8. Added hypoxic stimulus or electrical stimulation of the carotid sinus nerves caused an almost parallel increase of Phr(T) at all P(CO2) levels and all focal temperatures suggesting an additive type of interaction between the input from the peripheral chemoreceptors and that from the central (CO(2), H(+)) sensing structures whether the latter was altered by changing P(CO2) or by focal temperature changes on the I((S)) areas.9. In contrast to these effects of hypoxia and stimulation of the carotid sinus nerves the reflex increase of inspiratory activity caused by lung deflation or by electrical stimulation of the glossopharyngeal nerve distal to the carotid sinus nerves was CO(2) dependent. These reflex effects decreased with focal cooling of the I((S)) areas as with hypocapnia, suggesting a mainly multiplicative or ;gain-changing' type of interaction with the central chemoceptive drive.10. The close similarities in effect of focal cooling and of hypocapnia on the different respiratory parameters even during constant artificial ventilation indicate that focal temperature changes of the I((S)) areas intervene effectively with the normal ventilatory response to CO(2) without changing the chemical or physical environment of those neural structures in the brain stem which set respiratory pattern.

Animals↗

PubMed1975

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↗

PubMed1979

[Calculation of thermally caused blood flow changes in a finger using thermographic skin temperature measurements (author's transl)].

The skin temperature changes of the third finger were registered with the help of an infrared camera during a cooling process of the hand and forearm of a male, 38-years-old subject. Using the system of formulae, explained in previous publications [4-7], it was possible to describe the blood flow changes in the finger. The results are: 1. A formula for the "pseudo thermal conductivity" (material constant of the thermal conductivity plus the convective contribution), which is similar to the formula used for theat release of the whole body [4], describes well the experimental results. The "pseudo thermal conductivity" is a measure for the specific blood flow and can be converted into it. 2. The "pseudo thermal conductivity" has a local maximum. 3. The position of the maximum is independent of the tissue temperature. The anatomical properties of the finger seem to determine the position of the maximum. 4. The maximum of the "pseudo thermal conductivity"--and therefore the maximal blood flow--increases stronger than linearly with the tissue temperature.

Adult↗

PubMed1977

Fever produced in the rat by intracerebral E. coli endotoxin.

E. coli endotoxin introduced into the brain ventricles or into various brain areas raises the body temperature of conscious rats. Endotoxin-sensitive sites were found within the anterior hypothalamus and the lower brainstem. The increase in temperature (delta T) after microinjection of endotoxin into the anterior hypothalamic nucleus was dose-dependent. Endotoxin injected into the ventricles produced monophasic hyperthermia, but microinjections into the anterior hypothalamus produced monophasic or biphasic types of hyperthermia. The second and third microinjections of endotoxin into the anterior hypothalamic nucleus subsequently caused higher responses in delta T, but not in the rate of temperature change. The effects of the fourth and furter microinjections were the same as those of the third, and no tolerance developed for 24 days. The observations of behaviour, vegetative reactions, skin temperature, and carbon dioxide production indicated that the rise in the rat body temperature induced by endotoxin represents fever and that the heat is gained, at an ambient temperature of 22 degrees C, mainly through skin vessel vasoconstriction. Aspirin abolished and reversed fever induced by endotoxin, while hydrocortisone was without effect.

Animals↗

PubMed1976

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↗

PubMed1978

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↗

PubMed1978

Mechanims of extracellular acid-base regulation as temperature changes in decapod crustaceans.

In the crab Carcinus maenas, as in other decapod crustaceans, the extracellular pH varies with temperature so that the relative alkalinity remains approximately constant. However, as temperature changes, the blood acid-base behavior is not quite the same in an in vitro closed system and the living animal. In fully acclimated crabs, the higher the temperature, the lower the blood total CO2 concentration. After an abrupt temperature increase in vivo a new acid-base state is established instantaneously, comparable to that observed in vitro; but during the following hours, both PCO2 and bicarbonate concentration decrease concomitantly at constant pH. The relative gill ventilation, evaluated as the ratio of the ventilatory flow rate to the oxygen uptake rate, does not vary significantly as a function of temperature. No significant change in the base output can be detected during the hours following a temperature shift. These observations suggest that the mechanisms involved in the temperature-dependent acid-base regulation act mainly to control the blood bicarbonate level.

Acclimatization↗

PubMed1979

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↗

PubMed1979

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↗

PubMed1979

Hypothalamic thermo-responsive neurones in the new-born rat.

1. Single unit activities were recorded from the neurones in the preoptic area and anterior hypothalamus of developing new-born rats (aged 1-24 days old) during thermal stimulation of the brain. During the first 2 weeks of life, about 80% of these neurones had low spontaneous firing rates between 0.1 and 5 impulses/sec at 38 degrees C hypothalamic temperature (Thyp). 2. Out of 640 units studied, 118 units increased the firing rate upon elevation of Thyp (warm-units) and fourteen showed the opposite type of response to temperature changes (cold-units). Warm-units were found in the rats of all the age span studied and cold-units were recorded in the rats more than 8 days old. 3. Thermal coefficients of warm-units and cold-units varied between +0.11 and +2.47 and between -0.10 and -0.49 impulses/sec, degrees C, respectively. Number of warm-units with higher rates of firing and greater thermal coefficients, comparable to those of warm-units in the adult, gradually increased with growth. The thermal responsiveness of warm-units, when expressed by Q10, are already high even in the immediate neonatal period. Their Q10 values were in the range between 2 and 38.5 (mean 6.4). 4. Units responding to extrahypothalamic temperatures were only found in the rats more than 14 days old. 5. All the six warm-units tested increased the firing rates following subcutaneous injections of capsaicin, while the majority of thermo-unresponsive units were not affected by this drug. 6. It is suggested that thermo-responsive neurones in the preoptic area and anterior hypothalamus in the new-born rat have attained some degree of electrophysiological maturity, despite their slowly firing characteristics.

Action Potentials↗

PubMed1977

Aminergic and thermoregulatory mechanims in hypothalamic regulation of growth hormone in cats.

In conscious cats intravenous infusion of L-dopa (20 mg/kg) increased plasma growth hormone (GH), hydrocorticosterone (17-OHCS), and glucose while lowering midbrain (core) temperature (Tmb). Peripheral blockade of aromatic amino acid decarboxylase by L-alpha-hydrazino-methyldopa (MK 486) abolished only L-dopa hyperglycemia, indicating CNS stimulation by de novo catecholamines caused endocrine and temperature changes. Phenoxybenzamine but not pimozide pre-treatment abolished GH release after L-dopa. Apomorphine infusion alone did not alter basal GH. These data indicate central alpha-adrenergic mediation of GH release. Norepinephrine (NE) injected (5 or 10 microgram) into the preoptic anterior hypothalamus (POAH) (7 of 10 cases) and medial hypothalamus (17 of 30) raised GH while lowering Tmb, in agreement with alpha-adrenergic mediation. Responsive sites were distributed in ventral and dorsal medial hypothalamus and extended into the thalamus. Cooling of the POAH by implanted thermode raised GH in association with shivering, vasoconstriction, and rise in Tmb. Correlation between GH release and change in Tmb after L-dopa, central NE injection, and POAH cooling suggests hypothalamic integration of GH release with thermoregulation. Intravenous infusion of 5-hydroxytryptophan after MK 486 raised GH and 17-OHCS, suggesting serotonergic mechanisms also control GH and ACTH.

18-Hydroxycorticosterone↗

PubMed1979

Thermal quantification of region myocardial perfusion and heat generation.

A technique for experimental determination of regional myocardial blood flow and heat generation has been developed, based on a heat-clearance method. This method allows repetitive and frequent measurements of regional blood flow without necessity for biopsy or microspheres. Testing was performed on a pedicle preparation, an intact segment of left ventricular myocardium dependent on a single diagonal coronary artery and situated in situ in the left ventricular free wall. Total blood flow to the pedicle was measured by an electromagnetic flow probe. A specially designed 3-thermistor microprobe was positioned in the pedicle to continuously sense temperature changes in the subepicardium, midmyocardium, and subendocardium. The theory underlying this method is based on a heat balance that includes local myocardial heating, conduction, and convection. Comparison of the predicted time- and position-dependent temperature with that measured experimentally allows extraction of the local myocardial blood flow and heating rates. This method allows resolution of differential flows in subendocardial, midmyocardial, and subepicardial myocardium and provides quantification of dynamic flow changes in each layer in response to various stimuli such as ischemia or pressor agents, without in itself causing damage to the myocardial microvasculature. Our data show total flow, based on summation of thermally calculated regional flows, to have correlation coefficients of 0.88 with both the flowmeter and microsphere results. Resting flow values for Nembutal-anaesthetized, open-chest dogs of 0.66 ml/(g . min) compare favorably with values obtained by microsphere studies. Infusion of norepinephrine increased total flow and all layer flows, but the increase in subendocardial flow with norepinephrine was less than the increase of the other layers, perhaps accounting for the vulnerability of this region during catecholamine stress. Local myocardial heating rates in subepicardial, midendocardial, and subendocardial layers are shown to follow the same dependence on local myocardial blood flow in response to anoxic stress or norepinephrine-induced vasodilation. Specifically, local heating rate increases to a factor of 10 at flow below resting level.

Animals↗

PubMed1977

Hypoxia-induced metabolic and core temperature changes in the squirrel monkey.

To identify components of reduced core temperature (Tre) with exposure to hypoxia, oxygen uptake (VO2) and skin temperatures were measured in chair-restrained squirrel monkeys during conditions of 21% O2, 11% O2, and 11% O2 + 5% CO2. Exposure to 11% O2 resulted in a 20% decrease in VO2 and a 1.8 degrees C reduction of Tre with skin temperatures closely paralleling Tre. The addition of 5% CO2 to 11% O2 effectively blocked the decrease of both VO2 and Tre. The responses of one monkey (LD) exhibiting decreased Tre (greater than 2.0 degrees C) and 20% decrease in VO2 were compared to those of another (SD) exhibiting decreased Tre (less than 0.5 degrees C) and little change of VO2 under the same experimental conditions. Increased mean arterial blood pressure (BPa) and heart rate (HR) occurred for monkey SD, while for monkey LD BPa decreased and HR increased slightly. Arterial pressure of oxygen (PaO2) and calculated arterial saturation of oxygen (SaO2) were higher, while PaCO2 was lower for monkey SD than for monkey LD. When 5% CO2 was added to 11% O2 both animals exhibited decreased PaO2, little change of Tre, VO2, PaCO2, arterial pH, and calculated SaO2, and increased BPa and HR. These data suggest that decreased Tre resulted from reduced heat production and reduced oxygen transport was primarily responsible for reduction of heat production.

Animals↗

PubMed1979

D-tubocurarine requirement during hypothermia.

The effect of hypothermia on the action of d-tubocurarine (d-TC) was studied under carefully controlled experimental conditions. It was found that with computer controlled infusion, 60% less d-TC was required to sustain 75% muscle paralysis in cats, during steady-state, in vivo, when the temperature was changed from 37 degrees C to 30 degrees C. The corresponding relaxant consumption rates were 0.136 +/- 0.025 and 0.055 +/- 0.012 mg/kg/1/2 hr respectively. When there was no temperature change the maintenance dosage of d-TC remained constant for up to four hours denoting the equilibrium phase of the relaxant kinetics. Temperature transitions introduced dynamic changes in these kinetics and altered the constancy of the maintenance dosage.

Acetylcholine↗

PubMed1979

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↗

PubMed1979

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↗

PubMed1979

Skin temperature changes in paradoxical sleep in man in the cold.

Mean skin temperature (Tsk) calculated from seven sites and rectal temperature (Tre) were recorded every minute for a total of 88 man-nights in eight young men sleeping at night in both cold (during the Artic winter) and neutral (laboratory) environments, and were related to the EEG stages of sleep, especially to paradoxical sleep (PS). In the neutral environment, Tre was always above 36 degrees C and Tsk increased during PS. In the cold conditions, during PS, Tsk increased when Tre was high, and decreased when Tre was below 36 degrees C. It was concluded that, although it is not known why a core temperature of about 36 degrees C is the critical point of change in the direction of Tsk variations during PS, the direction in which Tsk will vary during PS is dependent on the core temperature at the time.

Adult↗