Stimulation of the nigrostriatal dopamine system inhibits both heat production and heat loss mechanisms in rats

1992 ◽  
Vol 346 (5) ◽  
Author(s):  
M.T. Lin ◽  
M.T. Ho ◽  
M.S. Young
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Dopamine System ◽  
Nigrostriatal Dopamine ◽  
Stimulation Of ◽  
Loss Mechanisms

Stimulation of the nigrostriatal dopamine system produces hypertension and tachycardia in rats

1994 ◽  
Vol 266 (6) ◽  
pp. H2489-H2496 ◽  
Author(s):  
M. T. Lin ◽  
J. J. Yang
Keyword(s):  
Corpus Striatum ◽  
Substantia Nigra Pars Compacta ◽  
Dopamine System ◽  
Arterial Blood ◽  
Nigrostriatal Dopamine ◽  
Induced Hypertension ◽  
Bilateral Vagotomy ◽  
6 Hydroxydopamine ◽  
Da Release ◽  
Stimulation Of

To test for the ability of the nigrostriatal dopamine (DA) system to influence cardiovascular function, experiments were carried out to assess the effects of electrical or chemical stimulation of the nigrostriatal DA system on arterial blood pressure, heart rate, and striatal DA release in anesthetized rats. Electrical stimulation of the substantia nigra pars compacta (SNC), in addition to enhancing the DA release in the corpus striatum (CS), elicited proportional hypertension and tachycardia. This could be mimicked by microinjection of two excitatory amino acids, kainic acid and glutamate, into the SNC area of rat brain. The SNC stimulation-induced hypertension, tachycardia, and increased striatal DA release were attenuated by prior destruction of the nigrostriatal DA system produced by intramedial forebrain bundle injection of 6-hydroxydopamine and by prior blockade of postsynaptic DA receptors produced by intra-CS injection of DA receptor antagonists, haloperidol or pimozide. The SNC stimulation-induced hypertension was attenuated by spinal transection, whereas the SNC stimulation-induced tachycardia was attenuated by bilateral vagotomy. The data suggest that stimulation of the nigrostriatal DA system produces both hypertension and tachycardia in rats.

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.

Thermal effects of dorsal head immersion in cold water on nonshivering humans

2005 ◽  
Vol 99 (5) ◽  
pp. 1958-1964 ◽  
Author(s):  
Gordon G. Giesbrecht ◽  
Tamara L. Lockhart ◽  
Gerald K. Bristow ◽  
Allan M. Steinman
Keyword(s):  
Heat Loss ◽  
Heat Production ◽  
Thermal Effects ◽  
Cold Water ◽  
The Body ◽  
Whole Body ◽  
Esophageal Temperature ◽  
Confounding Effect ◽  
Core Cooling ◽  
Stimulation Of

Personal floatation devices maintain either a semirecumbent flotation posture with the head and upper chest out of the water or a horizontal flotation posture with the dorsal head and whole body immersed. The contribution of dorsal head and upper chest immersion to core cooling in cold water was isolated when the confounding effect of shivering heat production was inhibited with meperidine (Demerol, 2.5 mg/kg). Six male volunteers were immersed four times for up to 60 min, or until esophageal temperature = 34°C. An insulated hoodless dry suit or two different personal floatation devices were used to create four conditions: 1) body insulated, head out; 2) body insulated, dorsal head immersed; 3) body exposed, head (and upper chest) out; and 4) body exposed, dorsal head (and upper chest) immersed. When the body was insulated, dorsal head immersion did not affect core cooling rate (1.1°C/h) compared with head-out conditions (0.7°C/h). When the body was exposed, however, the rate of core cooling increased by 40% from 3.6°C/h with the head out to 5.0°C/h with the dorsal head and upper chest immersed ( P < 0.01). Heat loss from the dorsal head and upper chest was approximately proportional to the extra surface area that was immersed (∼10%). The exaggerated core cooling during dorsal head immersion (40% increase) may result from the extra heat loss affecting a smaller thermal core due to intense thermal stimulation of the body and head and resultant peripheral vasoconstriction. Dorsal head and upper chest immersion in cold water increases the rate of core cooling and decreases potential survival time.

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.

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.

Stimulation of ventromedial hypothalamus induces cold defense responses in conscious rabbits

1986 ◽  
Vol 250 (4) ◽  
pp. R560-R566 ◽  
Author(s):  
A. Morimoto ◽  
N. Murakami ◽  
T. Ono ◽  
T. Watanabe ◽  
Y. Sakata
Keyword(s):  
Electrical Stimulation ◽  
Heat Loss ◽  
Heat Production ◽  
Defense Responses ◽  
Ventromedial Hypothalamus ◽  
O2 Consumption ◽  
Nonshivering Thermogenesis ◽  
Thermoregulatory Responses ◽  
Alpha Blockade ◽  
Stimulation Of

The involvement of the ventromedial hypothalamus (VMH) in thermoregulatory responses, which include heat production and heat loss responses, was investigated by the method of electrical stimulation. Electrical stimulation of the VMH caused a rise in rectal temperature, accompanied by the enhancement of heat production: O2 consumption and shivering. In addition, a reduction in heat loss was observed, including decreases in skin temperature (Ts), respiratory rate, and body surface area resulting from a huddled posture. In this study, stimulation of the lateral hypothalamus and other regions near the VMH had no effect on thermoregulatory responses. beta-Blocker (propranolol, 1 mg/kg iv) injected 20 min before stimulation lessened O2 consumption by approximately 10% and attenuated the reduction in Ts during VMH stimulation, whereas alpha-blockade (phentolamine, 1 mg/kg iv) was ineffective. These results indicate that most of the increase in O2 consumption during VMH stimulation was due to the occurrence of shivering but that some component of it could be due to nonshivering thermogenesis. They also indicate that the VMH, either directly or by converging influences, is involved in the activation of thermoregulatory responses to cold stress.

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
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