Biomedical subjects
Publications and source records attributed to M T Lin.
5,6-Dihydroxytryptamine, a serotonin depletor, infused directly into the anterior hypothalamus of rat's brain, produced an increase in both heat production and heat loss (as indicated by changes in peripheral circulation) at temperatures of 8, 15 and 22 degrees C. The rectal temperature of these treated rats remained constant.
The effects of intraventricular administration of beta-endorphin on thermoregulatory responses of unanesthetized rats to different ambient temperatures (Ta) of 8, 22 and 30 degrees C were assessed. Administration of beta-endorphin produced a fall in rectal temperature at both Ta 8 and 22 degrees C. The hypothermia in response to beta-endorphin was brought about by both cutaneous vasodilation (as indicated by an increase in both the tail and the foot skin temperatures) and decreases in metabolic heat production. However, at Ta 30 degrees C, administration of beta-endorphin produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermic effect induced by beta-endorphin was greatly attenuated by either the depletion of brain serotonin levels (with 5,6-dihydroxytryptamine and p-chlorophenylanine) or the blockade of opiate receptors (with naloxone). The data indicate that beta-endorphin leads to hypothermia in rats by increasing sensible heat loss and decreasing metabolic heat production, probably via the release of endogenous serotonin within brain.
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1. The effects of dopaminergic antagonist haloperidol and agonist apomorphine on the thermoregulatory responses of unanaesthetized rabbits to different ambient temperatures (Ta) of 2, 22 and 32 degrees C were assessed. 2. I.V. administration of haloperidol produced dose-dependent hypothermia at 2 and 22 degrees C Ta. At 2 degrees C Ta the hypothermia was due to a decrease in metabolic heat production. At 22 degrees C Ta the hypothermia was brought about by a decrease in metabolism and an increase in ear blood flow. However at 32 degrees C Ta, there was an increase in rectal temperature in response to haloperidol application; this hyperthermia was due to a decrease in both the ear blood flow and respiratory evaporative heat loss (Eres). 3. I.V. administration of apomorphine produced dose-dependent hyperthermia at all the ambient temperatures studied. At 2 degrees C Ta the hyperthermia was due to an increase in metabolism. At both 22 and 32 degrees C, the hyperthermia was brought about by an increase in metabolic heat production and a decrease in ear blood flow. Also, there was an increase in Eres in response to apomorphine at 22 degrees C Ta. 4. The data, in general, indicate that dopamine agonist activates all effector pathways which modulate the autonomic processes of thermoregulation (i.e. respiratory heat loss, peripheral vasomotor tone and metabolism), and that the dopamine antagonist inhibits the activity in all three effector pathways. Such a clear pattern of results is readily expressible in terms of the 'Bligh' model dealing with the aminergic mechanisms of temperature regulation.
1. The effects of beta-endorphin and morphine on thermoregulatory responses of unanaesthetized rabbits to different ambient temperatures (Ta) of 2, 22 and 32 degrees C were assessed. 2. Intraventricular administration of either beta-endorphin or morphine produced dose-dependent hypothermia at 2 and 22 degrees C Ta. At 2 degrees C Ta the hypothermia was brought about solely by a decrease in metabolic heat production. At 22 degrees C Ta the hypothermia was due to a decrease in metabolism and an increase in peripheral blood flow. However, at 32 degrees C Ta, there were no changes in rectal temperature in response to either beta-endorphin or morphine application. 3. Hypothermic effects of the administration of beta-endorphin or morphine were greatly antagonized by pretreatment of animals with either an opiate antagonist naloxone or a serotonin depletor 5,6-dihydroxytryptamine. 4. These findings indicate that the hypothermic responses to beta-endorphin or morphine in rabbits may be mediated through central serotonergic mechanisms. The hypothermia was due to a decrease in heat production and/or an increase in heat loss.
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Either systemic or central administration of apomorphine produced dose-related decreases in rectal temperature at ambient temperatures (Ta) of 8 and 22 degrees C in rats. At Ta = 8 degrees C, the hypothermia was brought about by a decrease in metabolic rate (M). At Ta = 22 degrees 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 degrees 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.
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 degrees C) and in the cold (8 degrees 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 degrees 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-hydroxydopamine (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 effects of acupuncture stimulation on the Ta-Chuei (Go-14), Nei-Kuan (EH-6), and Tsu-San-Li (St-36) loci on thermoregulatory function were assessed in normal adults. Stimulation of acupuncture locus Ta-Chuei produced hypothermia. The hypothermia was brought about by a decrease in metabolic rate, an increase in cutaneous circulation (the back region) and perspiration. On the other hand, acupuncture stimulation of either the Nei-Kuan or Tsu-San-Li loci produced a slight hyperthermia. The hyperthermia was due to a decrease in cutaneous circulation. The data indicate that each acupuncture locus may have its own function with special reference to body temperature regulation.
The vasopressor and bradycardia responses to an intravenous dose of epinephrine were assessed in saline-controlled, 5-hydroxytryptamine-(5-HT) depleted, and 5-HT-potentiated rats. Regardless of the previous treatment epinephrine produced an insignificant change in the basal levels of mean arterial pressure and heart rate. However, brain serotonin alteration did produce some influences on the reflex bradycardia in response to an elevation in arterial pressure. Elevating 5-HT contents in brain with 5-hydroxytryptophan (5-HTP) after peripheral decarboxylase inhibition with Ro 4-4602 produced a significant reduction in reflex bradycardia compared to the controls. In contrast, depleting 5-HT contents in brain with either p-chlorophenylalanine (PCPA) or 5,7-dihydroxytryptamine (5,7-DHT) led to an enhancement of epinephrine-induced bradycardia. Moreover, the enhanced reflex bradycardia induced by PCPA treatment was readily blocked by the replacement of the depleted brain 5-HT with 5-HTP and Ro 4-4602. The results suggest that serotoninergic systems play a role in the elaboration or modulation of reflex bradycardia. Specifically, 5-HT appears to inhibit reflex bradycardia since its depletion facilitated and its elevation inhibited reflex bradycardia.
Depressing functional serotonin or depleting serotonin levels in rat brains with either p-chlorophenylalanine, 5,6-dihydroxytryptamine or raphe lesions greatly enhanced hypothermia induced by chloropromazine (CPZ). Depressing the firing of raphe units or decreasing serotonin turnover in the brain with either a serotonin precursor (tryptophan) or the inhibitors of serotonin re-uptake (Lilly 1 10140 and chlorimipramine) also greatly enhanced the CPZ-induced hypothermia. The data indicate that serotonergic activity in the brain plays a role in the elaboration or modulation of CPZ hypothermia.
In rabbits, increasing serotonergic receptor activity or funtional serotonin in brain with either the inhibitors of serotonin reuptake (e.g. fluoxetine and chlorimipramine) or the serotonin precursor 5-hydroxytryptophan in combination with the peripheral decarboxylase inhibitor benserazide, greatly reduced the fever induced by intraventricular prostaglandin E1. The data indicate the brain serotonin plays a role in the elaboration or modulation of the prostaglandin E1-induced fever.
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 degrees, 28 degrees, and 41 degrees 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 or both the ventral thigh and the lateral lumbar regions at a TA of 41 degrees 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 vasodepressor and bradycardia responses of saline control, serotonin-depleted and serotonin-potentiated rats to an intravenous dose of prostaglandin E1 (PGE1) were assessed under the urethane anesthesia. Elevation of serotonin concentration in brain with either 5-hydroxytryptophan (a serotonin precursor) or chlorimipramine (an inhibitor of serotonin reuptake), although causing no changes in vasodepressor reuptake), although causing no changes in vasodepressor response, did enhance the PGE1-induced bradycardia in contrast, depleting serotonin concentration in brain with either p-chlorophenylalanine or 5,7-dihydroxytryptamine greatly reduced the PGE1-induced bradycardia without changes in vasodepressor response. Moreover, the reduced PGE1 bradycardia induced by p-chlorophenylalanine treatment was readily reversed by the replacement of the depleted brain serotonin with 5-hydroxytryptophan in combination with a peripheral decarboxylase inhibitor Ro4-4602. The data indicate that brain serotonergic systems play a role in the elaboration or modulation of the PGE1-induced bradycardia. Specifically, brain serotonin seems to facilitate the PGE1-induced bradycardia since its depletion causes a decrease and its potentiation or elevation causes an increase in the PGE1-induced bradycardia.
The effects of gamma-hydroxybutyric acid (GHBA) on metabolic, respiratory and vasomotor activities and body temperature were assessed in unanesthetized rats at three different ambient temperatures (Ta) of 8, 22 and 30 degrees C. Intraperitoneal administration of GHBA produced dose-dependent hypothermia in rats at both 8 and 22 degrees C Ta. At Ta = 8 degrees C the hypothermia was brought about solely by a decrease in metabolic heat production, while at Ta = 22 degrees C the hypothermia was due to both a decrease in metabolic heat production and an increase in cutaneous circulation (as indicated by changes in tail and foot skin temperatures). However, at Ta = 30 degrees C GHBA administration produced no changes in rectal temperature or other thermoregulatory parameters. Respiratory evaporative heat loss was not affected by GHBA application. Furthermore, it was found that the GHBA-induced hypothermia was antagonized by haloperidol (a selective blocker of dopamine receptors), but not by p-chlorophenylalanine (an inhibitor of serotonin synthesis). The data suggest that GHBA elicits a central dopamine receptor activation mainly via release of endogenous dopamine and leads to a hypothermia.
The effects of intraperitoneal administration of prostaglandin E1 (PGE1) on thermoregulatory responses were assessed in unanesthetized rats at ambient temperatures (Ta) of 8, 22 and 29 degrees C. The body temperatures, metabolic rate, respiratory evaporative heat loss and vasomotor activity in response to PGE1 were observed. Intraperitoneal administration of PGE1 produced dose-dependent hypothermia at Ta's of both 8 and 22 degrees C. The PGE1 hypothermia was due to both the decreased metabolic rate and the cutaneous vasodilation. However, at a Ta of 29 degrees C, intraperitoneal administration of PGE1 produced no changes in rectal temperature, since the thermoregulatory responses were not affected by PGE1 application at this Ta. The data indicate that peripheral administration of PGE1 decreases metabolic heat production and increases heat loss, which leads to hypothermia in rats, in contrast to hyperthermia seen after central administration.
The effects of intraperitoneal administration of sodium acetylsalicylate (aspirin) on thermoregulatory responses (Ta) of 15, 22 and 29 degrees C were assessed. Intraperitoneal administration of aspirin produced dose-dependent hypothermia at both 15 and 22 degrees C. The hypothermia was brought about by cutaneous vasodilation (as indicated by an increase of the tail and foot skin temperatures). However, in the heat (29 degrees C), i.p. administration of the same amount of aspirin produced no change in rectal temperature, since the thermo-regulatory responses were unaffected by aspirin application at this Ta. Thus it appears that aspirin increases heat loss and leads to hypothermia in rats.