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.

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.

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 apomorphine on thermoregulatory responses of rats to different ambient temperatures

1979 ◽  
Vol 57 (5) ◽  
pp. 469-475 ◽  
Author(s):  
M. T. Lin ◽  
Y. F. Chern ◽  
Zyx Wang ◽  
H. S. Wang
Keyword(s):  
Skin Temperature ◽  
Dopamine Neurons ◽  
Induced Hypothermia ◽  
Evaporative Heat Loss ◽  
Central Administration ◽  
Mean Skin Temperature ◽  
Ambient Temperatures ◽  
6 Hydroxydopamine ◽  
Sites Of Action ◽  
Skin Temperatures

Either systemic or central administration of apomorphine produced dose-related decreases in rectal temperature at ambient temperatures (Ta) of 8 and 22 °C in rats. At Ta = 8 °C, the hypothermia was brought about by a decrease in metabolic rate (M). At Ta = 22 °C, the hypothermia was due to an increase in mean skin temperature, an increase in respiratory evaporative heat loss (Eres) and a decrease in M. This increased mean skin temperature was due to increased tail and foot skin temperatures. However, at Ta = 29 °C, apomorphine produced increased rectal temperatures due to increased M and decreased Eres. Moreover, the apomorphine-induced hypothermia or hyperthermia was antagonized by either haloperidol or 6-hydroxydopamine, but not by 5,6-dihydroxytryptamine. The data indicate that apomorphine acts on dopamine neurons within brain, with both pre- and post-synaptic sites of action, to influence body temperature.

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 sweating in palmar hyperhidrosis before and after upper thoracic sympathectomy

1979 ◽  
Vol 50 (1) ◽  
pp. 88-94 ◽  
Author(s):  
Chun-Jen Shih ◽  
Mao-Tsun Lin
Keyword(s):  
Subcutaneous Administration ◽  
Atropine Sulfate ◽  
Normal Group ◽  
Palmar Hyperhidrosis ◽  
Surgical Removal ◽  
Content Type ◽  
Ambient Temperatures ◽  
Thoracic Sympathectomy ◽  
Normal Limits ◽  
Wide Range

✓ To assess thermoregulatory sweating in palmar hyperhidrosis, the authors determined the responses of three groups of normal, hyperhidrotic, and denervated subjects to a variety of ambient temperatures (TA's), 22°, 28°, and 41° C. The normal group had no hyperhidrosis, with intact T2–3 ganglia, the hyperhidrotic group had palm hyperhidrosis with intact T2–3 ganglia, and the denervated group had hyperhydrosis treated with T2–3 ganglionectomy. Both groups of hyperhidrotic and denervated subjects maintained oral and mean skin temperatures within normal limits displayed by the normal group over a wide range of TA's tested. The local sweating rate (LSR) of both the palms and the soles of the feet in the hyperhidrotic group was decreased to a minimal level by either the T2–3 ganglionectomy or the subcutaneous administration of atropine sulfate. Furthermore, the denervated group had a significantly lower LSR of both the forehead and the upper chest regions, but showed a higher LSR of both the ventral thigh and the lateral lumbar regions at a TA of 41° C when compared to the LSR of either the normal or the unoperated hyperhidrotic group. The data demonstrate that the surgical removal of both the T-2 and the T-3 ganglia, although producing no alterations in the thermal balance, does produce abnormalities in quantitative distribution of thermoregulatory sweating in man.

The effects of temperature and relative humidity on the thermoregulatory responses of grouped and isolated neonate chicks

1976 ◽  
Vol 86 (1) ◽  
pp. 35-43 ◽  
Author(s):  
B. H. Misson
Keyword(s):  
Body Size ◽  
Relative Humidity ◽  
Rectal Temperature ◽  
Heat Production ◽  
Water Loss ◽  
Evaporative Heat Loss ◽  
Evaporative Water ◽  
Ambient Temperatures ◽  
Metabolic Heat ◽  
Effects Of Temperature

SUMMARYMeasurements of O2 consumption (Vo2), CO2 production (VCO2) evaporative water loss and rectal temperature (Tr) have been made and metabolic heat production (H), evaporative heat loss (—E) and respiratory quotient (RQ) calculated with individual and groups of 1-day-old chicks at constant ambient temperatures (To) in the range 20—43 °C and 80 or 20% relative humidity (R.H.).Minimal metabolism (10·7 kJ/kgJ/h) occurred at 35 °C.One-day-old chicks act as heterotherms outside the zone of minimal metabolism since neither H nor —E are sufficiently developed mechanisms to maintain homeothermy.Huddling allows chicks to maintain a higher TT at a lower H per unit metabolic body size.Reducing E.H. from 80 to 20% raised the upper temperature survival limit (UTSL) from 41·5 to 43 °C.Panting was initiated when Ta = 38 °C and Tr was between 39·5 and 39·9 °C.

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.

Effect of ketamine on thermoregulation in rats

1978 ◽  
Vol 56 (6) ◽  
pp. 963-967 ◽  
Author(s):  
M. T. Lin ◽  
C. F. Chen ◽  
I. H. Pang
Keyword(s):  
Drug Treatment ◽  
Skin Temperature ◽  
Rectal Temperature ◽  
Heat Production ◽  
Intraperitoneal Administration ◽  
Metabolic Heat Production ◽  
Ambient Temperatures ◽  
Metabolic Heat ◽  
Dose Dependent ◽  
Skin Temperatures

Intraperitoneal administration of ketamine produced dose-dependent hypothermia at the ambient temperatures (Ta) of both 8 and 23 °C in unanesthetized rats. At a Ta of 8 °C, the hypothermia was brought about solely by a decrease in metabolic heat production. There were no changes in either the tail skin temperature (Ttail) or the sole skin temperature (Tsole). At a Ta of 23 °C, the hypothermia was due to an increase in Ttail, an increase in Tsole, and a decrease in metabolic heat production. However, at a Ta of 31 °C, there were no changes in rectal temperature in response to ketamine application, since neither heat production nor skin temperatures (e.g., Ttail and Tsole) was affected by ketamine at this Ta. The data indicate that the effect of the drug treatment may be to decrease heat production and (or) increase heat loss.

scholarly journals Systemic application of the TRPV4 antagonist GSK2193874 induces tail vasodilation in a mouse model of thermoregulation

2021 ◽  
Author(s):  
Fiona O'Brien ◽  
Caroline Staunton ◽  
Richard Barrett-Jolley
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Blood Vessels ◽  
Intraperitoneal Administration ◽  
Ambient Temperatures ◽  
Body Cooling ◽  
A Site ◽  
Systemic Application ◽  
Tail Blood

In humans the skin is a primary thermoregulatory organ, with vasodilation leading to rapid body cooling, whereas in rodents the tail performs an analogous function. TRPV4 is a widely distributed ion channel with both mechanical and thermosensitive properties. Previous studies have shown that TRPV4 can act as vasodilator by local action in blood vessels, and in this study we investigated whether there was a constitutive role for TRPV4 in mouse tail vascular tone and thermoregulation. We measured tail blood flow by pressure plethysmography in lightly sedated mice at a range of ambient temperatures, with and without intraperitoneal administration of the blood brain barrier crossing TRPV4 antagonist GSK2193874. We also measured heart rate and blood pressure with and without GSK2193874. As predicted, we found that tail blood flow increased with temperature. However, unexpectedly we found that the TRPV4 antagonist GSK2193874 increased tail blood flow at all temperatures. There were few detectable differences in heart rate, blood pressure or short-range heart rate variability. Since arterial TRPV4 activation is known to cause vasodilation that would increase tail blood flow, these data suggest that increases in tail blood flow resulting from the TRPV4 antagonist must arise from a site other than the blood vessels themselves, perhaps in central cardiovascular control centres such as the paraventricular nucleus of the hypothalamus.

Enhanced heat production in physically restrained rats in hypoxia

1981 ◽  
Vol 51 (6) ◽  
pp. 1601-1606 ◽  
Author(s):  
M. Hayashi ◽  
T. Nagasaka
Keyword(s):  
Blood Flow ◽  
Heat Production ◽  
Respiratory Muscles ◽  
Brown Adipose ◽  
Limb Muscles ◽  
Freely Moving ◽  
6 Hydroxydopamine ◽  
Colonic Temperature ◽  
Increased Blood Flow ◽  
Peak Value

Combined effects of restraint and hypoxia (9.5% O2 in N2) on heat production (M), heat loss (HL), colonic temperature (Tcol), and cardiovascular activity were studied in unanesthetized rats. In freely moving (F) rats, hypoxia decreased M, HL, Tcol, and heart rate (HR). In restrained (R) rats, however, hypoxia increased M, HL, Tcol, and HR. The increase in these parameters was greatest within 30 min of hypoxia, and the peak value of M was 10.4 W X m-2 higher than in normoxia. After chemical sympathectomy with 6-hydroxydopamine hydrobromide, no such increase was observed in R rats. l-Norepinephrine bitartrate (0.4 mg X kg-1) increased M and HR in F rats in hypoxia. The increase in M was, however, 9.5 W X m-2 and significantly less than that observed in normoxia. Hypoxia significantly reduced blood flow to the brown adipose tissues (BAT) in R rats. The BAT may not be responsible for the increased metabolism in restrained hypoxia-exposed rats. Hypoxia significantly increased blood flow to the heart and the diaphragm, and to a lesser extent to the limb muscles. The increased metabolism in the cardiac and respiratory muscles may be a cause of hyper-metabolism in restrained rats. The limb muscles may also play some role in increasing metabolism in these rats.

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