The role of the cholinergic systems in the central control of thermoregulation in rats

1979 ◽  
Vol 57 (11) ◽  
pp. 1205-1212 ◽  
Author(s):  
M. T. Lin ◽  
F. F. Chen ◽  
Y. F. Chern ◽  
T. C. Fung
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Nerve Fibers ◽  
Cholinergic Receptors ◽  
Evaporative Heat Loss ◽  
Central Administration ◽  
Ambient Temperatures ◽  
Dose Dependent ◽  
Selective Blocker

Systemic and central administration of methacholine (a synthetic choline derivative) both produced dose-dependent decreases in rectal temperature in rats at all the ambient temperatures studied. Both at room temperature (22 °C) and in the cold (8 °C), the hypothermia in response to methacholine application was brought about by both a decrease in metabolic heat production and an increase in cutaneous circulation. In the heat (29 °C), the hypothermia was due solely to an increase in respiratory evaporative heat loss. Furthermore, the methacholine-induced hypothermia was antagonized by central pretreatment of atropine (a selective blocker of cholinergic receptors), but not by the central administration of either 6-hydroxy-dopamine (a relative depletor of catecholaminergic nerve fibers) or 5,6-dihydroxytryptamine (predominately a serotonin depletor). The data indicate that activation of the cholinergic receptors within brain with methacholine decreases heat production and (or) increases heat loss which leads to hypothermia in rats.

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.

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.

Thermoregulatory effects of methoxamine and isoprenaline following injections into the cerebral ventricles of conscious rabbits

1977 ◽  
Vol 55 (4) ◽  
pp. 821-827 ◽  
Author(s):  
D. L. Jones ◽  
W. L. Veale ◽  
K. E. Cooper
Keyword(s):  
Body Temperature ◽  
Ambient Temperature ◽  
Heat Loss ◽  
Heat Production ◽  
Adrenergic Receptors ◽  
Cerebral Ventricles ◽  
Inhibitory Neurotransmitter ◽  
Ambient Temperatures ◽  
Hypothalamic Preoptic Area ◽  
Dose Dependent

There is evidence to suggest that within the hypothalamus noradrenaline (NA) is an inhibitory neurotransmitter acting on both the heat production and heat loss pathways in the rabbit. Further, it has been proposed that the inhibition of the heat loss pathway which results in hyperthermia is mediated primarily through α-adrenergic receptors within the anterior hypothalamic–preoptic area. We have investigated the effects of the α-receptor agonist methoxamine, administered directly into the cerebral ventricles, on body temperature at various ambient temperatures in both the shorn and unshorn rabbit. At all ambient temperatures tested, administration of methoxamine into a lateral cerebral ventricle produced a gradual dose-dependent hyperthermia. The magnitude of the hyperthermic response diminished with decreasing ambient temperatures. It is already known that the β-adrenergic agonist isoprenaline produces little or no effect on body temperature following intracranial application at ambient temperatures above 18 °C. In our experiments conducted at the lower ambient temperature, it produced a pronounced dose-dependent fall in body temperature in the shorn rabbit. The results of this work support the suggestion that NA can act as an inhibitory substance on the heat production or heat loss pathway in the rabbit. Which pathway is inhibited at any one time is dependent on the ambient temperature. Further, it would appear that inhibition of the heat loss pathway is largely mediated through α-adrenergic receptors, whilst the inhibition of the heat production pathway is mediated to a large extent through β-adrenergic receptors.

Pyrogenicity of interferon and its inducer in rabbits

1988 ◽  
Vol 254 (3) ◽  
pp. R499-R507 ◽  
Author(s):  
S. J. Won ◽  
M. T. Lin
Keyword(s):  
Heat Loss ◽  
Poly I:C ◽  
Evaporative Heat Loss ◽  
Hypothalamic Region ◽  
Ambient Temperatures ◽  
Intracerebral Administration ◽  
Protein Factor ◽  
Endogenous Release ◽  
Inhibitor Of Protein Synthesis ◽  
Dose Dependent

The effects of intracerebral administration of interferon (IFN) or its inducer polyriboinosinic acid-polyribocytidylic acid (poly I:C) on thermoregulatory responses were assessed in conscious rabbits. Administration of IFN (10(2)-10(6) IU) or poly I:C (0.012-12 micrograms) into the preoptic anterior hypothalamus or the third cerebral ventricle caused a dose-dependent fever in rabbits at three ambient temperatures (Ta) tested. In the cold (Ta = 8 degrees C), the fever was due to increased metabolism, whereas in the heat (Ta = 32 degrees C) the fever was due to a reduction in respiratory evaporative heat loss and ear skin blood flow. At the moderate environmental temperature (Ta = 22 degrees C), the fever was due to increased metabolism and cutaneous vasoconstriction. Compared with the febrile responses induced by cerebroventricular route injection of IFN or poly I:C, the hypothalamic route of injection required a much lower dose of IFN or poly I:C to produce a similar fever. Furthermore, the fever induced by intrahypothalamic injection of IFN or poly I:C was reduced by pretreatment of animals with a systemic dose of indomethacin (an inhibitor of all prostaglandins formation) or cycloheximide (an inhibitor of protein synthesis). The data indicate that IFN or its inducer may act through the endogenous release of a prostaglandin or a protein factor of an unknown chemical nature in the preoptic anterior hypothalamic region to induce fever in rabbits. The fever induced by IFN or its inducer is brought about by a decrease in heat loss and/or an increase in heat production in rabbits.

Serotoninergic Mechanisms of the Hypothermia Induced by Clerodenron Fragrans (Ventenaceae) in the Rat

1981 ◽  
Vol 09 (02) ◽  
pp. 144-154 ◽  
Author(s):  
Mao-Tsun Lin ◽  
Mei-Ling Ho ◽  
Andi Chandra ◽  
Hseng-Kuang Hsu
Keyword(s):  
Heat Loss ◽  
Adrenergic Receptors ◽  
Chinese Herb ◽  
Intraperitoneal Administration ◽  
Evaporative Heat Loss ◽  
Conscious Rats ◽  
Alpha Adrenergic Receptors ◽  
Cutaneous Vasodilatation ◽  
Dose Dependent ◽  
Selective Blocker

The effects of the Chinese herb Chou-Mou-Li, Clerodenron fragrans (Ventenaceae) on metabolic, respiratory and vasomotor activities as well as body temperatures were assessed in conscious rats at three different ambient temperatures (Ta) of 8, 22 and 30°C. Intraperitoneal administration of Chou-Mou-Li produced dose-dependent hypothermia in rats at both 8 and 22°C Ta. At 8°C Ta the hypothermia in response to Chou-Mou-Li was due to decreased metabolism, while at 22°C Ta the hypothermia was due to both decreased metabolism and cutaneous vasodilatation. There was no change in respiratory evaporative heat loss. Furthermore, the hypothermia induced by Chou-Mou-Li was greatly antagonized by pretreatment of animals with p-chlorophenylalanine (a selective depletor of brain serotonin), but not by either atropine sulfate (a selective blocker of cholinergic receptors), regitine (a selective blocker of alpha-adrenergic receptors) or DL-propranolol (a selective blocker of β-adrenergic receptors). However, at 30°C Ta, systemic administration of Chou-Mou-Li produced no change in rectal temperature or other thermoregulatory responses. On the other hand, direct administration of serotonin into the lateral cerebral ventricle of conscious rats also produced dose-dependent hypothermia at 8 and 22°C Ta. Again, the hypothermia in response to serotonin was due to decreased metabolism at 8°C Ta and was due to both decreased metabolism and cutaneous vasodilatation at 22°C Ta. At 30°C Ta administration of serotonin also produced no change in thermoregulatory functions. The data indicate that Chou-Mou-Li produces hypothermia by increasing sensible heat loss and decreasing metabolism heat production, probably via the release of endogenous serotonin within brain.

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.

Changes in serotonin contents in brain affect metabolic heat production of rabbits in cold

1978 ◽  
Vol 235 (1) ◽  
pp. R41-R47
Author(s):  
M. T. Lin ◽  
I. H. Pang ◽  
S. I. Chern ◽  
W. Y. Chia
Keyword(s):  
Blood Flow ◽  
Amino Acid ◽  
Heat Loss ◽  
Acid Decarboxylase ◽  
Evaporative Heat Loss ◽  
Decarboxylase Inhibitor ◽  
Ambient Temperatures ◽  
Amino Acid Decarboxylase ◽  
Metabolic Heat ◽  
Normal Limits

Elevating serotonin (5-HT) contents in brain with 5-hydroxytryptophan (5-HTP) reduced rectal temperature (Tre) in rabbits after peripheral decarboxylase inhibition with the aromatic-L-amino-acid decarboxylase inhibitor R04-4602 at two ambient temperatures (Ta), 2 and 22 degrees C. The hypothermia was brought about by both an increase in respiratory evaporative heat loss (Eres) and a decrease in metabolic rate (MR) in the cold. At a Ta of 22 degrees C, the hypothermia was achieved solely due to an increase in heat loss. Depleting brain contents of 5-HT with intraventricular, 5,7-dihydroxytryptamine (5,7-DHT) produced an increased Eres and ear blood flow even at Ta of 2 degrees C. Also, MR increased at all but the Ta of 32 degrees C. However, depleting the central and peripheral contents of 5-HT with p-chlorophenylalanine (pCPA) produced lower MR accompanied by lower Eres in the cold compared to the untreated control. Both groups of pCPA-treated and 5,7-DHT-treated animals maintained their Tre within normal limits. The data suggest that changes in 5-HT content in brain affects the MR of rabbits in the cold. Elevating brain content of 5-HT tends to depress the MR response to cold, while depleting brain content of 5-HT tends to enhance the MR response to cold.

Respiratory water and heat loss of the black duck during flight at different ambient temperatures

1971 ◽  
Vol 49 (5) ◽  
pp. 767-774 ◽  
Author(s):  
M. Berger ◽  
J. S. Hart ◽  
O. Z. Roy
Keyword(s):  
Heat Loss ◽  
Water Loss ◽  
Pulmonary Ventilation ◽  
Evaporative Heat Loss ◽  
Total Heat Loss ◽  
Ambient Temperatures ◽  
Black Duck ◽  
Respiratory Heat Loss ◽  
Metabolic Water ◽  
Expired Air

Pulmonary ventilation and temperature of expired air and of the respiratory passages has been measured by telemetry during flight in the black duck (Anas rubripes) and the respiratory water and heat loss has been calculated.During flight, temperature of expired air was higher than at rest and decreased with decreasing ambient temperatures. Accordingly, respiratory water loss as well as evaporative heat loss decreased at low ambient temperatures, whereas heat loss by warming of the inspired air increased. The data indicated respiratory water loss exceeded metabolic water production except at very low ambient temperatures. In the range between −16 °C to +19 °C, the total respiratory heat loss was fairly constant and amounted to 19% of the heat production. Evidence for the independence of total heat loss and production from changes in ambient temperature during flight is discussed.

Energy balance in ovariectomized rats with and without estrogen replacement

1980 ◽  
Vol 238 (5) ◽  
pp. R400-R405 ◽  
Author(s):  
M. L. Laudenslager ◽  
C. W. Wilkinson ◽  
H. J. Carlisle ◽  
H. T. Hammel
Keyword(s):  
Energy Balance ◽  
Heat Loss ◽  
Body Mass ◽  
Heat Production ◽  
Hormone Treatment ◽  
Ovariectomized Rats ◽  
Dark Phase ◽  
Evaporative Heat Loss ◽  
Estrogen Replacement ◽  
Dry Heat

The effect of estrogen replacement on several parameters of energy balance was investigated in ovariectomized rats tested during the dark phase of their diurnal cycle. Estrogen replacement, either as 17 beta-estradiol or beta-estradiol-3-benzoate via subcutaneous Silastic capsules, was associated with elevated rates of heat production and dry heat loss relative to untreated ovariectomized controls. Estrogen treatment reduced body mass and retarded fur growth. The effects of estrogen replacement on heat production and dry heat loss could not be attributed to these differences in body mass and fur growth or locomotor activity. Estrogen replacement had no effect on rate of evaporative heat loss. If estrogen replacement was delayed 75 days following ovariectomy, the increase in heat production and dry heat loss was not observed. There was no effect of the hormone treatment on rectal temperature. It was concluded that either heat production was elevated, with dry heat loss increased to compensate for the additional thermal load, or dry heat loss was accelerated with heat production elevated in compensation.

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