Intracerebroventricular injection of sympathomimetic drugs inhibits both heat production and heat loss mechanisms in the rat

1980 ◽  
Vol 58 (8) ◽  
pp. 896-902 ◽  
Author(s):  
M. T. Lin ◽  
A. Chandra ◽  
Y. F. Chern ◽  
B. L. Tsay
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Intracerebroventricular Injection ◽  
Ambient Temperatures ◽  
Adrenoceptor Antagonist ◽  
Sympathomimetic Drugs ◽  
Cutaneous Temperature ◽  
Behavioral Excitation ◽  
Cutaneous Vasoconstriction ◽  
Loss Mechanisms

The effects of intracerebroventricular (i.c.v.) injections of sympathomimetic drugs on thermoregulatory functions in conscious rats maintained at low (8 °C), moderate (22 °C), and high (30 °C) ambient temperatures were assessed. Norepinephrine, tyramine, and ephedrine each produced hypothermia at ambient temperature (Ta) 8 °C and hyperthermia at Ta 22 and 30 °C. At Ta 8 °C, the hypothermia in response to norepinephrine, tyramine, and ephedrine was due to decreased metabolic rate (M) whereas at Ta 22 °C the hyperthermia was due to cutaneous vasoconstriction. At Ta 22 °C, the hyperthermia in response to norepinephrine and tyramine was due to cutaneous vasoconstriction whereas the hyperthermia in response to ephedrine was brought about by increased M (due to behavioral excitation). Intracerebroventricular injection of epinephrine produced hypothermia followed by hyperthermia at Ta 8 and 22 °C. The hypothermia was due to decreased M whereas the hyperthermia was due to cutaneous vasoconstriction and increased M. At Ta 30 °C, epinephrine led to a reduction in cutaneous temperature and hyperthermia. Furthermore, i.c.v. administration of phenylephrine produced a decreased M and hypothermia at Ta, 8 °C and an increased M (due to behavioral excitation) and hyperthermia at Ta 30 °C. At Ta 22 °C, phenylephrine produced hyperthermia (due to cutaneous vasoconstriction and increased M) preceded by hypothermia (due to decreased M). Moreover, the temperature effects induced by norepinephrine were antagonized by pretreatment with the adrenoceptor antagonist phentolamine. In general, the data indicate that activation of central adrenoceptors with sympathomimetic drugs inhibits both heat production and heat loss mechanisms in the rat.

The catecholamine precursor L-3,4-dihydroxyphenylalanine inhibits both heat production and heat loss mechanisms in the rabbit

1980 ◽  
Vol 58 (8) ◽  
pp. 956-964 ◽  
Author(s):  
M. T. Lin
Keyword(s):  
Heat Loss ◽  
Intravenous Administration ◽  
Heat Production ◽  
Nerve Fibers ◽  
Evaporative Heat Loss ◽  
Intraventricular Administration ◽  
Ambient Temperatures ◽  
Behavioral Excitation ◽  
6 Hydroxydopamine ◽  
Loss Mechanisms

The effects of the catecholamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) on the thermoregulatory responses of conscious rabbits to different ambient temperatures (Ta) (2, 22, and 32 °C) were assessed. Intravenous administration of L-DOPA alone, intravenous administration of L-DOPA plus R04-4602 (a peripheral decarboxylase inhibitor), and intraventricular administration of L-DOPA or norepinephrine all produced a hypothermia at Ta 2 °C. The hypothermia was due to a decrease in metabolic heat production (M). On the other hand, L-DOPA or norepinephrine produced both behavioral excitation and hyperthermia at both Ta 22 and 32 °C. At Ta 22 °C, the hyperthermia was due to decreased ear skin blood flow (EBF) and slightly increased M (due to behavioral excitation) whereas at Ta 32 °C the hyperthermia was due to decreased EBF, decreased respiratory evaporative heat loss, and slightly increased M (due to behavioral excitation). Further, the temperature effects induced by L-DOPA were antagonized by pretreatment with 6-hydroxydopamine (a relative depletor of catecholaminergic nerve fibers) but not with haloperidol (a relative blocker of dopaminergic receptors). The data indicate that activation of central adrenergic receptors via the endogenous release of norepinephrine with L-DOPA inhibits both heat production and heat loss mechanisms in the rabbit.

Effects of intracerebroventricular injection of d-amphetamine on metabolic, respiratory, and vasomotor activities and body temperatures in the rat

1980 ◽  
Vol 58 (8) ◽  
pp. 903-908 ◽  
Author(s):  
M. T. Lin ◽  
A. Chandra ◽  
Y. F. Chern ◽  
B. L. Tsay
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Behavioral Responses ◽  
Nerve Fibers ◽  
Metabolic Heat Production ◽  
Evaporative Heat Loss ◽  
Central Administration ◽  
Metabolic Heat ◽  
Behavioral Excitation ◽  
Cutaneous Vasoconstriction

Systemic and central administration of d-amphetamine both produced dose-dependent hypothermia in the rat at ambient temperature (Ta) 8 °C. The hypothermia was brought about solely by a decrease in metabolic heat production. However, at both Ta 22 and 30 °C, d-amphetamine produced hyperthermia accompanied by behavioral excitation. The hyperthermia was due to cutaneous vasoconstriction and increased metabolic heat production (due to behavioral excitation) at Ta 22 °C, whereas at Ta 30 °C the hyperthermia was due to cutaneous vasoconstriction, decreased respiratory evaporative heat loss, and increased metabolism (due to behavioral excitation). Furthermore, both the thermal and the behavioral responses induced by d-amphetamine were antagonized by pretreatment with intracerebroventricular administration of 6-hydroxydopamine (a depletor of central catecholaminergic nerve fibers). The data indicate that, by eliminating the interference of behavioral responses induced, d-amphetamine leads to an alteration in body temperature of rats by decreasing both metabolic heat production and sensible heat loss, probably via the activation of central catecholaminergic receptors.

Effects of bombesin on thermoregulatory responses and hypothalamic neuronal activities in the rat

1986 ◽  
Vol 251 (2) ◽  
pp. R303-R309
Author(s):  
K. S. Lin ◽  
M. T. Lin
Keyword(s):  
Heat Loss ◽  
Rectal Temperature ◽  
Heat Production ◽  
The Other ◽  
Single Neurons ◽  
Hypothalamic Area ◽  
Ambient Temperatures ◽  
Thermoregulatory Responses ◽  
Cutaneous Temperature ◽  
Direct Administration

Direct administration of bombesin (1, 10, and 100 ng/microliter) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures (Ta) of 8 and 22 degrees C. The hypothermia in response to bombesin was brought about by a decrease in metabolism at Ta 8 degrees C, whereas at Ta 22 degrees C the hypothermia was brought about by both a decrease in metabolism and an increase in cutaneous temperature. However, at Ta 30 degrees C, intrahypothalamic administration of bombesin caused an insignificant change in thermoregulatory responses. On the other hand, 51 single neurons in the preoptic anterior hypothalamic area were examined in 20 rats under urethan anesthesia. Each animal was subjected to scrotal warming or cooling and to the administration of bombesin. Microiontophoretic application of bombesin resulted in inhibition of the majority (62.5%) of cold-responsive neurons as well as excitation of the majority (50%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (74%) of thermally unresponsive neurons were not affected by bombesin application. The data indicate that bombesin, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.

Angiotensin II inhibits both heat production and heat loss mechanisms in the rat

1980 ◽  
Vol 58 (8) ◽  
pp. 909-914 ◽  
Author(s):  
M. T. Lin ◽  
A. Chandra ◽  
J. J. Jou
Keyword(s):  
Angiotensin Ii ◽  
Heat Loss ◽  
Heat Production ◽  
Ambient Temperatures ◽  
Thermoregulatory Responses ◽  
Adrenergic Antagonist ◽  
Intracerebroventricular Injections ◽  
6 Hydroxydopamine ◽  
Dose Dependent ◽  
Loss Mechanisms

The effects of intracerebroventricular injections of angiotensin II on thermoregulatory responses of conscious rats to ambient temperatures (Ta) of 8, 22, and 30 °C were assessed. Administration of angiotensin II produced dose-dependent hypothermia in rats at both Ta 8 and 22 °C. The hypothermia in response to angiotensin II was due to decreased metabolic heat production. In addition, angiotensin II produced cutaneous vasoconstriction at Ta 8–22 °C. However, at Ta 30 °C angiotensin II produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermia induced by angiotensin II was antagonized by pretreatment with 6-hydroxydopamine (a selective catecholamine neurotoxin) and propranolol (a selective β-adrenergic antagonist) but not by either 5,6-dihydroxytryptamine (a selective serotonin neurotoxin), atropine (a cholinergic antagonist), or phentolamine (a selective α-adrenergic antagonist). The data indicate that angiotensin II inhibits both heat production and heat loss mechanisms which lead to an alteration in body temperature, probably via the activation of central adrenergic receptors.

Effects of phentolamine on thermoregulatory functions of rats to different ambient temperatures

1979 ◽  
Vol 57 (12) ◽  
pp. 1401-1406 ◽  
Author(s):  
M. T. Lin ◽  
Andi Chandra ◽  
T. C. Fung
Keyword(s):  
Heat Loss ◽  
Rectal Temperature ◽  
Heat Production ◽  
Room Temperature ◽  
Metabolic Heat Production ◽  
Central Component ◽  
Evaporative Heat Loss ◽  
Central Administration ◽  
Ambient Temperatures ◽  
Metabolic Heat

The effects of both systemic and central administration of phentolamine on the thermoregulatory functions of conscious rats to various ambient temperatures were assessed. Injection of phentolamine intraperitoneally or into a lateral cerebral ventricle both produced a dose-dependent fall in rectal temperature at room temperature and below it. At a cold environmental temperature (8 °C) the hypothermia in response to phentolamine was due to a decrease in metabolic heat production, but at room temperature (22 °C) the hypothermia was due to cutaneous vasodilatation (as indicated by an increase in foot and tail skin temperatures) and decreased metabolic heat production. There were no changes in respiratory evaporative heat loss. However, in the hot environment (30 °C), phentolamine administration produced no changes in rectal temperature or other thermoregulatory responses. A central component of action is indicated by the fact that a much smaller intraventricular dose of phentolamine was required to exert the same effect as intraperitoneal injection. The data indicate that phentolamine decreases heat production and (or) increases heat loss which leads to hypothermia, probably via central nervous system actions.

Thermoregulatory and metabolic changes during fever in young and old rats

2003 ◽  
Vol 285 (5) ◽  
pp. R1165-R1169 ◽  
Author(s):  
Jessica B. Buchanan ◽  
Elizabeth Peloso ◽  
Evelyn Satinoff
Keyword(s):  
Metabolic Rate ◽  
Heat Loss ◽  
Heat Production ◽  
Metabolic Changes ◽  
Body Temperatures ◽  
Ambient Temperatures ◽  
Young Rats ◽  
Heat Conservation ◽  
Old Rats ◽  
S Peak

We injected old and young rats with lipopolysaccharide (LPS; 50 μg/kg ip) at two ambient temperatures ( Ta; 21 and 31°C). Young rats mounted equivalent fevers at both Tas [peak body temperatures ( Tb) of 38.3 and 38.7°C, respectively]. The Tbof old rats was not different from baseline (37.3°C) after LPS at Ta21°C, whereas, at 31°C, their Tbrose to a mean peak of 38.4°C. We also measured the associated thermoregulatory responses by use of calorimetry. At 21°C, young rats developed a fever by increasing both O2consumption and heat conservation. Old rats did not become febrile, and O2consumption fell by 15%. Heat loss was the same in old and young rats. At 31°C, young and old rats developed similar fevers with similar increases in heat production and conservation. Our results suggest that the lack of LPS fever in old rats at 21°C is due mainly to the lowered metabolic rate.

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

1982 ◽  
Vol 242 (5) ◽  
pp. R471-R481 ◽  
Author(s):  
M. T. Lin ◽  
A. Chandra ◽  
B. L. Tsay ◽  
Y. F. Chern
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Direct Injection ◽  
Receptor Activation ◽  
Anterior Hypothalamus ◽  
Evaporative Heat Loss ◽  
Dopaminergic Agonist ◽  
Striatal Dopamine Receptor ◽  
Cutaneous Vasoconstriction ◽  
Intrahypothalamic Injection

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.

Temperature regulation in the new-born lamb. III. Effect of environmental temperature on metabolic rate body temperatures, and respiratory quotient

1961 ◽  
Vol 12 (6) ◽  
pp. 1152 ◽  
Author(s):  
G Alexander
Keyword(s):  
Body Temperature ◽  
Heat Loss ◽  
Heat Production ◽  
Temperature Regulation ◽  
Low Temperatures ◽  
Environmental Temperature ◽  
Body Temperatures ◽  
Normal Body Temperature ◽  
Ambient Temperatures ◽  
New Born

Studies were made on temperature regulation of lambs in a closed circuit indirect calorimeter. Dry new-born lambs were able to maintain normal body temperature in ambient temperatures as low as -5°C. This was accomplished by increasing heat production to 2–3 times "basal" levels, apparently by increased oxidation of fats, and by reducing heat loss through the extremities by vasoconstriction. The lower limit of the zone of thermal neutrality was about 29°C. In unsuckled lambs within 24 hr of birth, the heat produced in response to cold appeared to be independent of pre-natal nutrition and age. It was considerably lower in lambs with hairy coats than in lambs with fine coats. Milk intake increased heat production, and this increase was abolished after 12 hr of fasting in lambs up to 3 days old, but the increase persisted in older lambs. The increase was accompanied by, and was apparently due to, elevated heat loss from the extremities, which persisted even at low temperatures. The maximal thermal insulation of the tissues, calculated from these results, was about 1 Clo; that of the fleece plus air was only 1 to 2 Clo.

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