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 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.

Mechanisms of thermal stability during flight in the honeybee apis mellifera

1999 ◽  
Vol 202 (11) ◽  
pp. 1523-1533 ◽  
Author(s):  
S.P. Roberts ◽  
J.F. Harrison
Keyword(s):  
Thermal Stability ◽  
Heat Loss ◽  
Heat Production ◽  
Radiative Heat ◽  
Carbon Dioxide Production ◽  
Metabolic Heat Production ◽  
Evaporative Heat Loss ◽  
Radiative Heat Loss ◽  
Convective Heat Loss ◽  
Metabolic Heat

Thermoregulation of the thorax allows honeybees (Apis mellifera) to maintain the flight muscle temperatures necessary to meet the power requirements for flight and to remain active outside the hive across a wide range of air temperatures (Ta). To determine the heat-exchange pathways through which flying honeybees achieve thermal stability, we measured body temperatures and rates of carbon dioxide production and water vapor loss between Ta values of 21 and 45 degrees C for honeybees flying in a respirometry chamber. Body temperatures were not significantly affected by continuous flight duration in the respirometer, indicating that flying bees were at thermal equilibrium. Thorax temperatures (Tth) during flight were relatively stable, with a slope of Tth on Ta of 0.39. Metabolic heat production, calculated from rates of carbon dioxide production, decreased linearly by 43 % as Ta rose from 21 to 45 degrees C. Evaporative heat loss increased nonlinearly by over sevenfold, with evaporation rising rapidly at Ta values above 33 degrees C. At Ta values above 43 degrees C, head temperature dropped below Ta by approximately 1–2 degrees C, indicating that substantial evaporation from the head was occurring at very high Ta values. The water flux of flying honeybees was positive at Ta values below 31 degrees C, but increasingly negative at higher Ta values. At all Ta values, flying honeybees experienced a net radiative heat loss. Since the honeybees were in thermal equilibrium, convective heat loss was calculated as the amount of heat necessary to balance metabolic heat gain against evaporative and radiative heat loss. Convective heat loss decreased strongly as Ta rose because of the decrease in the elevation of body temperature above Ta rather than the variation in the convection coefficient. In conclusion, variation in metabolic heat production is the dominant mechanism of maintaining thermal stability during flight between Ta values of 21 and 33 degrees C, but variations in metabolic heat production and evaporative heat loss are equally important to the prevention of overheating during flight at Ta values between 33 and 45 degrees 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.

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.

scholarly journals Sex-related differences in local and whole-body heat loss responses: Physical or physiological?

2014 ◽  
Vol 39 (7) ◽  
pp. 843-843
Author(s):  
Daniel Gagnon
Keyword(s):  
Sex Differences ◽  
Heat Loss ◽  
Heat Production ◽  
Experimental Studies ◽  
Metabolic Heat Production ◽  
Whole Body ◽  
Fixed Rate ◽  
The Third ◽  
Metabolic Heat ◽  
Body Heat

The current thesis examined whether sex differences in local and whole-body heat loss are evident after accounting for confounding differences in physical characteristics and rate of metabolic heat production. Three experimental studies were performed: the first examined whole-body heat loss in males and females matched for body mass and surface area during exercise at a fixed rate of metabolic heat production; the second examined local and whole-body heat loss responses between sexes during exercise at increasing requirements for heat loss; the third examined sex-differences in local sweating and cutaneous vasodilation to given doses of pharmacological agonists, as well as during passive heating. The first study demonstrated that females exhibit a lower whole-body sudomotor thermosensitivity (553 ± 77 vs. 795 ± 85 W·°C−1, p = 0.05) during exercise performed at a fixed rate of metabolic heat production. The second study showed that whole-body sudomotor thermosensitivity is similar between sexes at a requirement for heat loss of 250 W·m−2 (496 ± 139 vs. 483 ± 185 W·m−2·°C−1, p = 0.91) and 300 W·m−2 (283 ± 70 vs. 211 ± 66 W·m−2·°C−1, p = 0.17), only becoming greater in males at a requirement for heat loss of 350 W·m−2 (197 ± 61 vs. 82 ± 27 W·m−2·°C−1, p = 0.007). In the third study, a lower sweat rate to the highest concentration of acetylcholine (0.27 ± 0.08 vs. 0.48 ± 0.13 mg·min−1·cm−2, p = 0.02) and methacholine (0.41 ± 0.09 vs. 0.57 ± 0.11 mg·min−1·cm−2, p = 0.04) employed was evidenced in females, with no differences in cholinergic sensitivity. Taken together, the results of the current thesis show that sex itself can modulate sudomotor activity, specifically the thermosensitivity of the response, during both exercise and passive heat stress. Furthermore, the results of the third study point towards a peripheral modulation of the sweat gland as a mechanism responsible for the lower sudomotor thermosensitivity in females.

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.

Effect of 5-hydroxytryptamine and acetylcholine on the energy budget of chickens

1980 ◽  
Vol 239 (1) ◽  
pp. R57-R61
Author(s):  
P. E. Hillman ◽  
N. R. Scott ◽  
A. van Tienhoven
Keyword(s):  
Physical Activity ◽  
Heart Rate ◽  
Body Temperature ◽  
Heat Loss ◽  
Energy Budget ◽  
Heat Production ◽  
Evaporative Heat Loss ◽  
Neural Pathways ◽  
Metabolic Heat ◽  
Intraventricular Injections

Intraventricular injections of 5-hydroxytryptamine-HCl (258 nmol) or acetylcholine-HCl (550 nmol) in the chicken caused body temperature to rise at 35 degrees C ambient, a result of decreased evaporative heat loss due to bradypnea. At 10 and 20 degrees C ambient, neither drug affected body temperature. Although these drugs decreased physical activity or shivering or both at 10 and 20 degrees C, metabolic heat production was not depressed enough to alter body temperature significantly. Heart rate decreased simultaneously with decreased activity at 20 degrees C. This study is the first to inject 5-hydroxytryptamine as a salt of HCl, instead of creatinine sulfate, as is commonly used. It is suggested that some of the differences reported herein, compared to other studies, are due to the type of salt used. It is postulated that either 5-hydroxytryptamine or acetylcholine, rather than norepinephrine, may be an important neurotransmitter in the neural pathways for thermoregulation in chickens, even though their action on thermoregulation is minor compared with norepinephrine.

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