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.

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 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 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.

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 brain monoamine depletion on chlorpromazine-induced hypothermia in rabbits

1979 ◽  
Vol 57 (1) ◽  
pp. 16-23 ◽  
Author(s):  
M. T. Lin
Keyword(s):  
Blood Flow ◽  
Heat Production ◽  
Intraperitoneal Administration ◽  
Induced Hypothermia ◽  
Evaporative Heat Loss ◽  
Ambient Temperatures ◽  
Normal Limits ◽  
Wide Range ◽  
Monoamine Depletion ◽  
6 Hydroxydopamine

The thermal responses of three groups of control, 6-hydroxydopamine (6-OHDA) treated and 5,7-dihydroxytryptamine (5,7-DHT) treated rabbits to the administration of chlorpromazine (CPZ) were assessed at three different ambient temperatures (Ta: 2, 22, and 32 °C). Depleting catecholamines (CA) in brain with 6-OHDA produced a decrease in metabolic rate, in respiratory evaporative heat loss, and in ear blood flow at both Ta's of 2 and 22 °C, while depleting 5-hydroxytryptamine (5-HT) contents in brain with 5,7-DHT produced the opposite responses at the same Ta's. However, these amine-depleted animals maintained their rectal temperatures within normal limits over a wide range of Ta's tested. Furthermore, intraperitoneal administration of CPZ produced hypothermia at both Ta's of 2 and 22 °C. The major cause of the CPZ-induced hypothermia was an inhibition of metabolic heat production at Ta of 2 °C. At Ta of 22 °C, the CPZ-induced hypothermia was due to both a decrease in heat production and an increase in ear blood flow. However, CPZ hypothermia was attenuated in the CA-depleted animals, but was potentiated in the 5-HT-depleted animals. The data indicate that brain monoamines are involved in the central mechanisms of CPZ-induced hypothermia.

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.

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.

Evaporative Heat Loss Mechanisms of the Newborn Calf, Bos Taurus

1968 ◽  
Vol 124 (2) ◽  
pp. 83-88 ◽  
Author(s):  
J.R.S. Hales ◽  
J.D. Findlay ◽  
D. Robertshaw
Keyword(s):  
Heat Loss ◽  
Bos Taurus ◽  
Evaporative Heat Loss ◽  
Loss Mechanisms

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.

Sign in / Sign up

Export Citation Format

Share Document