Heat Production In Rats Research Articles

Dynamics of locomotor activity and heat production in rats after acute stress.

The dynamics of locomotor activity and heat production were studied in rats demonstrating passive and active behavior in the open field test at different time after exposure to acute emotional stress caused by 12-h immobilization during dark hours. The most pronounced changes in behavior and heat production followed by disturbances in circadian rhythms of these parameters were detected within the first 2 days after stress. In contrast to behaviorally active rats, the most significant decrease in locomotor activity and heat production of passive animals subjected to emotional stress was observed during dark hours. Circadian rhythms of behavior and heat production in rats tended to recover on day 3 after immobilization stress. These data illustrate the specificity of metabolic and behavioral changes reflecting the shift of endogenous biological rhythms in individuals with different prognostic resistance to stress at different terms after exposure to negative emotiogenic stimuli.

Influence of the hypothalamus on the midbrain tonic inhibitory mechanism on metabolic heat production in rats

Influence of the hypothalamus on increased body temperature was examined in male rats. Body temperature was increased by removing the midbrain tonic inhibitory mechanism (TIM) on heat production from brown adipose tissue (BAT) by microinjections of a local anesthetic, procaine, into the midbrain. Procaine microinjections in unanesthetized rats increased rectal temperature that was followed by a strong tail skin temperature rise. Procaine microinjections in unanesthetized and decerebrated rats also increased rectal temperature but without skin temperature rise. These decerebrated animals fatally developed hyperthermia. In anesthetized rats, procaine microinjections increased temperature of the interscapular BAT (IBAT) higher with shorter onset for temperature rise than rectal temperature. Increased IBAT temperature by procaine microinjections in anesthetized rats was attenuated during hypothalamic warming, and enhanced during hypothalamic cooling when compared with that observed during thermoneutral hypothalamic temperature. These results suggest that the midbrain TIM is able to function in unanesthetized conscious rats, and that the integrity of the midbrain mechanism to tonically inhibit metabolic heat production does not require the presence of intact hypothalamus. These results also suggest that the hypothalamus modulates directly or indirectly IBAT heat production that was induced by removal of the midbrain TIM.

Involvement of sympathetic activation and brown adipose tissue in calcitonin gene-related peptide-induced heat production in the rat

We previously reported that microinjection of calcitonin gene-related peptide (CGRP; 1.6–8.0 pmol, 0.2–1.0 μl) into the ventromedial hypothalamus (VMH) increased oxygen consumption ( VO 2), heart rate (HR), colonic temperature ( T co), and temperature of interscapular brown adipose tissue ( T IBAT). In the present study, we investigated whether the autonomic nervous system is involved in the CGRP-induced heat production in urethane-anesthetized rats. Intraperitoneal administration of the ganglion blocker hexamethonium (20 mg/kg) or the β-adrenergic antagonist propranolol (5 mg/kg) suppressed the CGRP-induced increases in VO 2, HR, T co, and T IBAT. Pretreatment with the α-adrenergic antagonist phentolamine (5 mg/kg) partly attenuated the heat production response but did not affect the tachycardiac response. Bilateral sectioning of the nerves supplying the IBAT attenuated the CGRP-induced increase in T IBAT but not significantly that in VO 2 or T co. In rats with adrenal demedullation, the effects of CGRP were similar to those in intact rats. These results suggest that the CGRP-induced heat production is mediated by the sympathetic nervous system and, at least in part, by the BAT through the α- and β-adrenoceptors.

Locomotor Activity and Heat Production of Rats on Restricted Two-Hour Feeding Regimes

Locomotor Activity and Heat Production of Rats on Restricted Two-Hour Feeding Regimes

Blood flow to brown fat in lean and obese adrenalectomized Zucker rats.

The Zucker obese rat is characterized by decreased capacity for diet-induced and for nonshivering thermogenesis. This decrease is due, in large part, to reduced thermogenesis in depots of brown adipose tissue, a major source of heat production in rats. Adrenalectomy retards the weight gain observed in the obese rats and also normalizes brown fat guanosine 5'-diphosphate (GDP) binding, an in vitro measure of brown fat thermogenic capacity. This study examined the effect of adrenalectomy on brown fat blood flow, an in vivo measure of the tissue's function, and on norepinephrine-induced O2 consumption (NST) of 11-wk-old obese (fa/fa) and lean (Fa/?) rats. Adrenalectomy had little effect on weight gain, NST, or norepinephrine-stimulated blood flow to brown fat in lean rats. However, adrenalectomy produced profound changes in the obese animals, preventing the weight gain normally occurring in the obese rats and normalizing both NST capacity and norepinephrine-stimulated blood flow to brown fat. These findings provide further support for the importance of brown fat thermogenesis and glucocorticoids in modulating the obesity of the Zucker rat.

Striatal neuronal responses to scrotal temperature changes and dopaminergic drugs.

Seventy-nine units in the striatal region were examined in 48 urethan-anesthetized rats. When these units were classified by their thermal responsiveness, proportions of the cold-responsive, warm-responsive, and thermally unresponsive units were 25.4, 35.4, and 39.2%, respectively, of the total units tested. Either microiontophoretically or systemically administered apomorphine (a dopamine agonist) and haloperidol (a dopamine antagonist) affected (inhibited and/or excited) most (86.5-100%) cold-responsive units. In contrast, only a small percentage of the warm-responsive (28.6-43.8%) or thermally unresponsive (0-19.2%) units were affected by both apomorphine and and haloperidol. Furthermore it was found that most (73-100%) cold-responsive units were inhibited by apomorphine but excited by haloperidol; the inhibitory responses of the unit activity induced by apomorphine were antagonized by haloperidol. The reciprocal relationships between apomorphine and haloperidol were not observed in most warm-responsive (76.2-85.7%) or thermally unresponsive (80.8-100%) units. The data demonstrate that many striatal neurons are influenced by thermal afferent activation in the scrotum. The results also provide a neuronal basis for the hypothesis that the dopaminergic receptors located in the cold-responsive neurons of the striatum have effects on metabolic heat production in rats.

Effects of restraint on baroreflex sensitivity in altering heart rate and heat production in rats.

When systemic arterial pressure was elevated with phenylephrine (PHE) at 13 degrees C, heart rate (HR), and heat production (M) associated with shivering were greatly suppressed in rats. The magnitude of suppression increased proportionally with increasing doses of PHE. During restraint, however, such a suppression of HR and M with PHE was attenuated, indicating that restraint reduced baroreflex sensitivity in altering HR and shivering in rats.

Hypothalamic and striatal dopamine receptor activation inhibits heat production in the rat.

Direct injection of dopaminergic agonist apomorphine into the lateral cerebral ventricle, the preoptic anterior hypothalamus, the caudate-putamen complex, or the globus pallidus caused hypothermia, decreased metabolism and cutaneous vasoconstriction at ambient temperature (Ta) 8 and 22 degrees C, and hyperthermia and cutaneous vasoconstriction in the rat at Ta 30 degrees C. On the other hand, local injection of dopaminergic antagonists such as haloperidol and pimozide into the preoptic anterior hypothalamus and the striatal nuclei caused hyperthermia, increased metabolism and cutaneous vasoconstriction at Ta 8, 22, and 30 degrees C. However, there was no change in respiratory evaporative heat loss in response to administration of either dopaminergic agonist or antagonists in the rat at all Ta studied. The data indicate that hypothalamic and striatal dopaminergic receptor activation inhibits metabolic heat production in rats. In addition, intrahypothalamic injection of 5-hydroxytryptamine caused hypothermia, decreased metabolism and cutaneous vasodilatation in the rat at Ta 8 and 22 degrees C, whereas at Ta 30 degrees C caused an insignificant change in the thermoregulatory responses. Furthermore, the thermal responses induced by intrahypothalamic injection of apomorphine were not altered by depletion of hypothalamic 5-hydroxytryptamine. These observations do not support the contention that there is a dopamineserotonin link in the hypothalamic pathways that mediate heat loss mechanisms in the rat.

Bioenergetics of thermogenesis: Effects of some neurotropic drugs on heat production

1. 1. DDT is able to stimulate heat production in rats independently on central thermal receptors. 2. 2. Chlorpromazine and imipramine decreased the hyperthermic effect of DDT on intact as well as decapitated rats. 3. 3. DDOH blocked completely oxygen consumption by mitochondria pretreated with chlorpromazine or imipramine. 4. 4. DDOH reversed the passive swelling of mitochondria induced by chlorpromazine or imipramine in KCl and NaCl solutions. 5. 5. Dearrangement of mitochondrial membrane permeability to osmotically active cations as a mode of anti-hyperthermic action of chlorpromazine or imipramine on peripherial heat production stimulated by DDT is discussed.

The heat production of rats fed isocaloric and protein-equivalent diets with different proportions of fat to carbohydrates.

The heat production of rats fed isocaloric and protein-equivalent diets with different proportions of fat to carbohydrates.

Influence of Low, Intermediate and High Levels of Dietary Protein on Heat Production of Rats

An experiment was performed in which 28 young, growing male albino rats were fed diets based upon casein, glucose monohydrate and lard plus corn oil as the protein, carbohydrate and fat sources, respectively. The 4 diets, essentially isocaloric and containing approximately 8, 25, 41 and 57% protein, were fed in equal quantities within each of 7 quadruplicates of animals for a 53-day period with total collection of excreta. Carcasses of experimental animals, diets and excreta were analyzed for nitrogen and energy. Weight gain, feed efficiency and the N, energy and dry matter of the weight gain were at maximal values at the 25% level of dietary protein. The N of feces and urine increased with increasing percentage of dietary protein. Digested energy tended to remain constant, but metabolized energy decreased with increasing percentage of dietary protein above 25% protein. The specific dynamic effect of the food and the total heat production (gross energy of food minus the sum of energy of excreta and energy of the weight gain) of the animals decreased as the dietary protein increased from 8 to 25% and then increased as the dietary protein increased from 25 to 57%. The compatibility of these results with the general principle that the optimal overall utilization of a diet will occur when all required nutrients are at optimal levels was pointed out. The applicability of the general observations to the interpretation of results of similar studies involving human subjects was suggested.