The effects on thermoregulation of intracerebroventricular injections of acetylcholine, pilocarpine, physostigmine, atropine and hemicholinium in the rat.
Explore the source record for details and available documents.
Acetylcholine↗
Biomedical subjects
M T Lin
Publications and source records attributed to M T Lin.
Naloxone produces hypothermia in rats pretreated with beta-endorphin and morphine.
Explore the source record for details and available documents.
Animals↗
The effects of theophylline and caffeine on thermoregulatory functions of rats at different ambient temperatures.
Both systemic and central administration of theophylline and caffeine produced a dose-dependent rise in rectal temperature at ambient temperatures of 8, 22 and 30 degrees C. The hyperthermia in response to either xanthine was brought about by an increase in metabolic heat production. In addition, their administration produced behavioral excitation, cutaneous vasodilation (as estimated by an increase in the foot and tail skin temperatures) and diuresis. There was no change in respiratory evaporative heat loss. Probably, the hyperthermia induced by the two drugs was due to behavioral excitation leading to an increased metabolism at the ambient temperatures studied. Furthermore, either destruction of central catecholaminergic nerve fibres (with 6-hydroxydopamine) or blockade of alpha-adrenergic and dopaminergic (with phentolamine and haloperidol) receptors antagonized the xanthine-induced hyperthermia. The data suggest that these xanthines elicit a central activation of both adrenergic and dopaminergic receptors via release of endogenous catecholamines that leads to behavioral excitation and hyperthermia in rats.
Animals↗
The catecholamine mechanisms of prostaglandin E1-induced hypothermia in rats.
Intraperitoneal administration of prostaglandin E1 (PGE1) produced a hypothermia in rats at room temperatue (22 degrees C). The hypothermia in response to PGE1 was due to cutaneous vasodilatation and decreased metabolic heat production. Depletion of brain 5-hydroxytryptamine (with 5,6-dihydroxytryptamine and p-chlorophenylalanine) did not alter the PGE1-induced hypothermia. However, depletion of bran catecholamines (with 6-hydroxydopamine) and blockade of central catecholaminergic receptors (with phentolamine and propranolol) both greatly reduced the PGE1-induced hypothermia. The data indicate that PGE1 lowers body temperature in rats by acting on the central catecholaminergic systems.
Animals↗
Effects of 5-hydroxytryptamine, fluoxetine and chlorimipramine on reflex bradycardia in rats.
In the urethane-anaesthetized rat, increasing 5-hydroxytryptaminergic receptor activity or functional 5-HT in brain with either the specific inhibitors of 5-HT reuptake (e.g. fluoxetine and chlorimipramine) or the 5-HT itself greatly reduced the reflex bradycardia induced by the systemically administered adrenaline. The data indicate that activation of central 5-HT-ergic receptors tends to inhibit reflex bradycardia.
Animals↗
Regional distribution of sodium acetylsalicylate in the brain of normothermic and hyperthermic rabbits.
This study was designed to determine regional distribution of sodium acetylsalicylate in the brain of normothermic rabbits, rabbits with hyperthermia induced by pyrogen administration, and rabbits with hyperthermia induced by infrared irradiation. Increasing body temperature with either leucocytic pyrogen or infrared light irradiation about doubled the concentration of sodium acetylsalicylate in four regions of the brain. This suggests a more rapid penetration of sodium acetylsalicylate into the brain under hyperthermic conditions. This may explain why the drug lowers body temperature more effectively in febrile animals than in afebrile animals.
Animals↗
Intracerebroventricular injection of sympathomimetic drugs inhibits both heat production and heat loss mechanisms in the rat.
The effects of intracerebroventricular (i.c.v.) injections of sympathomimetic drugs on thermoregulatory functions in conscious rats maintained at low (8 decrees C), moderate (22 degrees C), and high (30 degrees C) ambient temperatures were assessed. Norepinephrine, tyramine, and ephedrine each produced hypothermia at ambient temperature (Ta) 8 degrees C and hyperthermia at Ta 22 and 30 degrees C. At Ta 8 degrees, the hypothermia in response to norepinephrine, tyramine, and ephedrine was due to decreased metabolic rate (M) whereas at Ta 22 degrees C the hyperthermia was due to cutaneous vasoconstriction. AT Ta 22 degrees 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 degrees C. The hypothermia was due to decreased M whereas the hyperthermia was due to cutaneous vasoconstriction and increased M. AT Ta 30 degrees C, epinephrine led to a reduction in cutaneous temperature and hyperthermia. Furthermore, i.c.v. administration of phenylephrine produced a decreased M and hypothermia Ta 8 degrees C and an increased M (due to behavioral excitation) and hyperthermia at Ta 30 degrees C. At Ta 22 degrees 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.
Animals↗
Effects of intracerebroventricular injection of d-amphetamine on metabolic, respiratory, and vasomotor activities and body temperatures in the rat.
Systemic and central administration of d-amphetamine both produced dose-dependent hypothermia in the rat at ambient temperature (Ta) 8 degrees C. The hypothermia was brought about solely by a decrease in metabolic heat production. However, at both Ta 22 and 30 degrees 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 degrees C, whereas at Ta 30 degrees 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.
Animals↗
Angiotensin II inhibits both heat production and heat loss mechanisms in the rat.
The effects of intracerebroventricular injections of angiotensin II on thermoregulatory responses of conscious rats to ambient temperatures (Ta) of 8, 22, and 30 degrees C were assessed. Administration of angiotensin II produced dose-dependent hypothermia in rats at both Ta 8 and 22 degrees 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 degrees C. However, at Ta 30 degrees C angiotensin II produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermia induced by angiotension II was antagonized by pretreatment with 6-hydroxytryptamine (a selective catecholamine neurotoxin) and propranolol (a selective beta-adrenergic antagonist) but not either 5,6-dihydroxytryptamine (a selective serotonin neurotoxin), atropine (a cholinergic antagonist), or phentolamine (a selective alpha-adrenergic antagonist). The data indicate that angiotension 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.
5,6-Dihydroxytryptamine↗
The catecholamine precursor L-3,4-dihydroxyphenylalanine inhibits both heat production and heat loss mechanisms in the rabbit.
The effects of catecholamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) on the thermoregulatory responses of conscious rabbits to different ambient temperatures (Ta) (2, 22, and 30 degrees 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 degrees 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 degrees C. At Ta 22 degrees C, the hyperthermia was due to decreased ear skin blood flow (EBF) and slightly increased M (due to behavioral excitation) whereas at Ta 32 degrees C the hyperthermia was due to 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 endogeneous release of norepinephrine with L-DOPA inhibits both heat production and heat loss mechanisms in the rabbit.
Animals↗
Effects of brain monoamine depletions on thermoregulation in rabbits.
Biochemical analyses revealed that 5,7-dihydroxytryptamine- (5,7-DHT) treated and 6-hydroxydopamine- (6-OHDA) treated rabbits, respectively, had a significant reduction in diencephalic 5-hydroxytryptamine (5-HT) and norepinephrine (NE) with minimal alterations in the other monoamines. Both 5,7-DHT-treated and 6-OHDA-treated animals, although showing the maintenance of normal body temperatures, did exhibit specific alterations in the thermoeffector outputs. The 5-HT-depleted animals displayed an increase in ear skin blood flow, respiratory heat loss, and metabolism at both ambient temperatures (Ta) of 22 and 2 degrees C. The NE-depleted animals displayed a decrease in metabolism at all levels of Ta tested. Also, the peripheral temperature threshold for the onset of heat loss responses were displaced to higher values than in control animals. In addition, the prostaglandin E1-induced fever was attenuated after the pretreatment of rabbits with either 5,7-DHT or 6-OHDA. The data indicate that brain levels of 5-HT and NE alter, in an apparently reciprocal fashion, the thermoregulatory responses of rabbits. Also, the integrity of 5-HT and NE pathways in brain is vital for the full functioning of a prostaglandin in producing a fever.
5,7-Dihydroxytryptamine↗
Serotoninergic mechanisms of beta-endorphin- and clonidine-induced analgesia in rats.
Both beta-endorphin and clonidine proved to have statistically significant analgesic activity (increase in latency to hind-paw lick in hot plate test) in rats. Furthermore, the pain inhibition induced by beta-endorphin and clonidine could be antagonized by prior treatment of animals with either naloxone (a narcotic antagonist) or the depletors of central serotonin pathways such as 5,6-dihydroxytryptamine, 5,7-dihydroxytryptamine and p-chlorophenylalanine have not effect on latency to hind-paw lick. The data indicate that serotoninergic activity in the brain plays a role in the elaboration or modulation of beta-endorphin and clonidine analgesia in rats.
5,6-Dihydroxytryptamine↗
Effects of methacholine and acetylcholine on metabolic, respiratory, vasomotor and body temperature responses in rabbits.
Central administration of methacholine and acetylcholine each produced a dose-dependent hypothermia in conscious rabbits at room temperature (22 degrees C) and below. At room temperature, hypothermia in response to methacholine and acetylcholine was due to decreased metabolism and increased heat loss (both an increase in ear skin blood flow and in respiratory evaporative heat loss). In the cold (4 degrees C), hypothermia was brought about by a decrease in metabolic heat production and an increase in respiratory evaporative heat loss. However, in the heat (32 degrees C), central administration of methacholine and acetylcholine each produced a dose-dependent hyperthermia in rabbits. The hyperthermia was due to a decrease in both ear skin blood flow and respiratory evaporative heat loss. Furthermore, the effects of methacholine of acetylcholine on body temperature was antagonized by pretreatment with atropine.
Acetylcholine↗
Effects of Chinese herb, Huang Chin (Scutellaria baicalensis George) on thermoregulation in rats.
Intragastric administration of a Chinese herb, Huang Chin extract (Scutellaria baicalensis George), produced a dose-dependent fall in rectal temperature in conscious rats in a room the temperature of which was 22 degrees C or below. The hypothermia in response to Huang Chin application was brought about solely by cutaneous vasodilatation (as estimated by an increase in cutaneous temperatures). There were no changes in either metabolic heat production or respiratory evaporative heat loss. However, in the heat (29 degrees C), Huang Chin administration produced no changes in rectal temperature or other thermoregulatory responses. The data indicate that Huang Chin extract produces peripheral vasodilatation which leads to a hypothermia in conscious rats.
Animals↗
Effects of cholinomimetic drugs on sudomotor, metabolic, respiratory, vasomotor, and temperature response in palmar hyperhidrosis.
The effects of cholinomimetic drugs such as mecholyl (methacholine) and pilocarpine on autonomic functions (including sudomotor, metabolic, respiratory, vasomotor, and temperature responses) were assessed at room temperature (24 degrees C) in three groups of individuals, including normal, hyperhidrotic, and denervated subjects. The normal group had no palmar hyperhidrosis, with intact T2-3 ganglia, the hyperhidrotic group had palmar hyperhidrosis with intact T2-3 ganglia, and the denervated group had palmar hyperhidrosis treated with T2-3 ganglionectomy. Subcutaneous administration of mecholyl and pilocarpine each produced a fall in oral temperature in the normal group. The hypothermia was brought about by a decrease in metabolic rate, an increase in local sweating rate (mainly of the upper limb and trunk), and an increase in cutaneous circulation (estimated by an increase in the upper limb and trunk skin temperatures). The autonomic functions induced by these cholinomimetic drugs were antagonized by pretreatment with atropine sulfate (an antagonist of cholinergic receptors). Moreover, the hypothermia induced by mecholyl or pilocarpine was greatly reduced in the hyperhidrotic group. The reduction in the cholinomimetic-induced hypothermia in the hyperhidrotic group was due to the reduced sudomotor and metabolic responses after the injections of these cholinomimetic drugs, as compared to those of the normal group. However, neither the excessive sweating of the palms nor the reduced cholinergic responses in the hyperhidrotic group was observed after T2-3 ganglionectomy. The data indicate that the T2-3 ganglia play a role in the elaboration or modulation of the sudomotor and metabolic responses induced by activation of certain cholinergic receptors in humans.
Adult↗
Effects of dopamine, apomorphine gamma-hydroxybutyric acid, haloperidol and pimozide on reflex bradycardia in rats.
The cardiovascular responses to i.v. doses of epinephrine were assessed in vehicle-controlled, dopamine-treated, apomorphine-treated, gamma-hydroxybutyric acid-treated, haloperidol-treated and pimozide-treated rats, under urethan anesthesia. Previous exposure to several injections of epinephrine did not change the basal values of arterial pressure and heart rate. It was found that dopaminergic transmission alterations within the brain did produce some influence on the reflex bradycardia in response to an elevation in arterial pressure. Blockade of dopaminergic receptors in brain with either haloperidol or pimozide produced a significant recution in reflex bradycardia compared to the controls. In contrast, either direct activation of central dopamine receptors witth dopamine and apomorphine or indirect activation of central dopamine receptors with gamma-hydroxybutyric acid led to an enhancement in epinephrine-induced bradycardia. The data indicate that central dopmaine systems play a role in the elaboration or modulation of reflex bradycardia. Specifically, brain dopamine appears to facilitate reflex bradycardia since activation of dopamine systems facilitated and blockade inhibited reflex bradycardia.
Animals↗
Haloperidol produces hypothermic effects in rats.
Intraperitoneal administration of either haloperidol or chlorpromazine produced hypothermia both in the cold (8 degrees C) and at room temperature (22 degrees C). The hypothermia was brought about both by a decrease in metabolic heat production and an increase in the cutaneous temperature of tail and foot skin. However, at a higher temperature (29 degrees C), there were no changes in rectal temperature and other thermoregulatory responses.
Animals↗
Severe combined immune-deficiency disease in patient with alpha 1-antitrypsin deficiency.
Explore the source record for details and available documents.
Dysgammaglobulinemia↗