The regulation of respiratory evaporative heat loss in the rabbit.

1. Respiratory evaporative heat loss in the rabbit has a minimum value of 0-2-0-3 W/kg and a maximum value of about 1-1 W/kg in non-evaporatively limited environments. 2. Both skin temperature and hypothalamic temperature influence respiratory evaporative heat loss, and they do so in a multiplicative fashion. Thus, at low skin temperature the hypothalamic temperature threshold for the onset of panting is above normal hypothalamic temperature and hypothalamic thermosensitivity is high. On the other hand, at high skin temperatures, the hypothalamic temperature threshold for the onset of panting is well below normal hypothalamic temperature, but hypothalamic thermosensitivity is greatly reduced. 3. The influence of mean skin temperature (Tsk) and hypothalamic temperature on respiratory evaporative heat loss (Eres) in the rabbit can be described by the equation: Eres=1-1-0-08 (Tsk-39-7) (Thy-42-9) greater than or equal to 0-3 W/kg. 4. Thus, the ability of a lowered mean skin temperature to increase the thermosensitivity of the hypothalamus in response to local temperature changes applies to heat loss mechanisms as well as heat production mechanisms. It is suggested that the characteristics of this peripheral input into the C.N.S. are fulfilled by tonic cold fibre input originating from the peripheral cold receptors on the body surface.     

Laryngeal water receptors are insensitive to body temperature in neonatal piglets

Heat stress and the laryngeal chemoreflex (LCR) have both been implicated as possible contributors to the sudden infant death syndrome (SIDS). We recently reported that moderate hyperthermia, induced in decerebrate piglets by external heating, substantially prolonged the LCR elicited by injecting 0.1 ml of water into the larynx through a prepositioned transnasal catheter. To examine the question of whether hyperthermia influences the responses of laryngeal water receptors, we recorded single fiber action potentials in fine strands of the superior laryngeal nerve (SLN) in decerebrate piglets while the larynx was filled with water or isotonic saline. Water receptors, identified by their much brisker response to water than to saline, were studied with body temperature at 37.9+/-0.2 degrees C, after warming the animal to 40.6+/-0.2 degrees C and after cooling back to 37.7+/-0.3 degrees C. The results show no effect of body temperature change, in this range, on the responses of the laryngeal water receptors and thus suggest that the potentiation of the LCR by hyperthermia is mediated by a central action.     

Sex differences in mouse heart rate and body temperature and in their regulation by adenosine A1 receptors

Aim: To examine cardiac function, body temperature and locomotor behaviour in the awake adenosine A₁ receptor knock out mouse of both sexes. Methods: Male and female A₁R (+/+) and (−/−) mice, instrumented with telemetric devices, were recorded during basal conditions and after drug administration. Results: Female mice had higher heart rate, body temperature and locomotion, both during daytime and during the night. Awake A₁R (−/−) mice had a slightly elevated heart rate, and this was more clear‐cut in males. Heart rate was also higher in Langendorff‐perfused denervated A₁R (−/−) hearts. Body temperature was higher in A₁R (−/−) males and females; locomotor activity was higher in A₁R (−/−) females, but not in males. The adenosine receptor agonist R‐PIA (0.2 mg kg⁻¹) decreased heart rate and body temperature, but less in A₁R (−/−) animals than in A₁R (+/+) mice (P < 0.001 in both parameters). The unselective adenosine receptor antagonist caffeine had a minor stimulatory effect on heart rate in lower doses, but depressed it at a dose of 75 mg kg⁻¹. Body temperature was increased after a low dose (7.5 mg kg⁻¹) of caffeine in both sexes and genotypes, and markedly reduced after a high dose (75 mg kg⁻¹) of caffeine. An intermediary dose of caffeine 30 mg kg⁻¹ increased or decreased body temperature depending on genotype and sex. Locomotor responses to caffeine were variable depending both on genotype and sex. Conclusion: Thus, the adenosine A₁ receptor is involved in the regulation of heart rate, body temperature and locomotor activity, but the magnitude of the involvement is different in males and females.     

Early experience facilitates the development of temperature regulation in the cat

Thirty kittens were given a 30-min exposure to a moderately cool environment and drop in body temperature was measured. One group was tested every day from age 2 days to 21 days of age. A 2nd group was tested on Days 6–21 and a 3rd group tested only at 19 days of age. The 1st group (tested on Days 2–21) became homeothermic at an earlier age than did the other groups. The data are interpreted to indicate that early exposure to cool temperatures facilitates acquisition of temperature regulation in the cat, and that observed deficits in passive avoidance learning in young cats are not due to increased motor activity produced by a fall in body temperature.     

Biphasic changes in body temperature produced by intracerebroventricular injections of histamine in the cat.

1. Intracerebroventricular administration of histamine to cats caused hypothermia followed by a rise in body temperature. 2-Methylhistamine caused a similar biphasic response, while 3-methylhistamine had no effect on body temperature and 4-methylhistamine produced a delayed hyperthermia. Some tolerance to the hypothermic activity developed when a series of closely spaced injections of histamine was given. 2. Doses of histamine and 2-methylhistamine which altered body temperature when given centrally were ineffective when infused or injected I.V. 3. Pyrilamine, an H1-receptor antagonist, prevented the hypothermic response to histamine. 4. Hypothermic responses to histamine at an environmental temperature of 22 degrees C were comparable to responses in a cold room at 4 degrees C in both resting animals and animals acting to depress a lever to escape an external heat load. A change in error signal from the thermostat could account for these results. However, lesser degrees of hypothermia developed when histamine was given to animals in a hot environment. In some, but not all animals, this smaller response could be attributed to inadequate heat loss in spite of maximal activation of heat-loss mechanisms. 5. The hyperthermic response to histamine was antagonized by central, but not peripheral, injection of metiamide, an H2-receptor antagonist. 6. The results indicate that histamine and related agents can act centrally to cause both hypothermia, mediated by H1-receptors, and hyperthermia, mediated by H2-receptors.     

The significance of changes in the temperature of the skin and body core of the chicken in the regulation of heat loss

1. The relationship between the temperatures of the hypothalamus, colon and skin and the control of heat loss mechanisms at ambient temperatures from 20 to 40 degrees C has been studied in unanaesthetized chickens.2. The temperatures of the core and feathered skin varied by not more than 5 degrees C throughout the full range of ambient temperature but the comb, shank and toe varied by up to 20 degrees C and exhibited wide fluctuations in constant environmental conditions.3. At an ambient temperature of 26-27 degrees C, the fluctuations ceased at all of the naked skin sites and there was evidence of a concurrent decrease in the tissue insulation of the extremities. No such change could be detected in the feathered skin.4. Analysis of the various body temperatures suggested that the onset of thermal panting was consistently related to the increment in hypothalamic temperature and that this relationship was influenced both by the peripheral and extra-cranial deep body temperatures.     

Environmental light and suprachiasmatic nucleus interact in the regulation of body temperature

The mammalian biological clock, located in the suprachiasmatic nucleus (SCN), is crucial for circadian rhythms in physiology and behavior. However, equivocal findings have been reported on its role in the circadian regulation of body temperature. The goal of the present studies was to investigate the interaction between the SCN and environmental light in the regulation of body temperature. All recordings were performed by telemetry in free moving male Wistar rats. Firstly, we demonstrated an endogenous circadian rhythm in body temperature independent of locomotor activity. This rhythm was abolished by stereotactic lesioning of the SCN. Secondly, we demonstrated a circadian phase-dependent suppressive effect of light ('negative masking') on body temperature. Light suppressed body temperature more at the end of the subjective night (circadian time [CT] 22) than in the middle (CT 6) and at the end (CT 10) of the subjective day. This circadian-phase dependent suppression was not demonstrated in SCN-lesioned animals. Surprisingly, after half a year of recovery from lesioning of the SCN, light regained its suppressing action on body temperature, resulting in a daily body temperature rhythm only under light-dark conditions. In contrast to body temperature, light could not substantially mimic a daytime inhibitory SCN-output in the regulation of heart rate and locomotor activity. The present results suggest that, after lesioning of the SCN as main relay station for the immediate body temperature-inhibition by light, secondary relay nuclei can fully take over this function of the SCN. These findings provide a possible explanation for the controversy in literature over the question whether the SCN is required for the diurnal rhythm in body temperature. Furthermore, they show that light may have an acute effect on behavior and physiology of the organism via the SCN, which extends beyond the generally acknowledged effect on melatonin secretion.     

Atrial receptors in the cat.

Action potentials were recorded from slips of the cervical vagi in anaesthetized cats. Single functional units with atrial patterns of discharge (type A, B and Intermediate) were first obtained and then attempts were made to alter (i.e. convert) their patterns of discharge. Finally the points of origin of their action potentials were located. The investigations were done in five stages. 2. In the first series, thirty unselected units were investigated in thirty cats. Twenty-five of these were located in the endocardium of vein-atrial system and consisted of two type A, fifteen type B and eight Intermediate type units. The remaining five units were located elsewhere in the chest Conversion of the pattern of discharge was achieved in sixteen of the twenty-five atrial units. Both atrial type A units were converted. 3. In the second series, eight type A units were selectively studied in twelve cats. Five were located in the atrial endocardium and all were converted. Of the other three units which were located at other sites in the chest, one could not be converted. 4. In the third series, four type A units which could not be converted were selectively studied in twenty cats. All were located outside the atria. 5. In the fourth series, three type B units which could not be converted were selectively studied in six cats. These units were located in the pulmonary veins and in the lateral walls of the atria. 6. In the fifth series, fifty-five units were investigated in three anaesthetized spontaneously breathing cats. The proportion of the types of units were similar to that obtained in the artificially respired cats (first series). 7. The present study has shown that atrial receptors with a type A pattern of discharge are relatively rare in the cat and that conversion of the patterns of discharge is a common phenomenon. Evidence is presented which suggests that there is one basic type of atrial receptor whose pattern of discharge is determined by their precise location in the vein-atrial system.     

Divergent action of verapamil perfused in two hypothalamic areas on body temperature of the cat

Guide cannulae for push-pull perfusion were bilaterally implanted stereotaxically within the anterior hypothalamic, preoptic area (AH/POA) and posterior hypothalamus (PH) of the cat. Catecholamine-reactive sites were identified within AH/POA in which a microinjection of norepinephrine (NE) (5.0 micrograms) evoked a characteristic, transient hypothermia. Similarly the cation-reactive region within the PH was identified in which excess Ca2+ (25 mM) also evoked a hypothermic response. When verapamil was perfused at a rate of 25.0 microliters/min in a concentration of 0.4 or 2.0 micrograms/microliter within AH/POA at a NE-sensitive site, a concentration-dependent decline in the core temperature of the cat occurred. Conversely, verapamil perfused in the same manner with a Ca2+-reactive site caused an intense rise in the cat's body temperature which also was concentration dependent. These results show that the localized blockade of slow Ca2+ channels exerts direct, differential physiological effects within central nervous system tissue. In this case, verapamil mimics noradrenergic effects within the AH/POA; however, the hyperthermic response following Ca2+ channel blockade within tissue of the PH resembled that produced by ethyleneglycoltetraacetic acid or Na ions.