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Biomedical subjects

M T Lin

Publications and source records attributed to M T Lin.

At least 289 records · Page 16Linked to original sources
PubMed1983

A prostaglandin-adrenergic link occurs in the hypothalamic pathways which mediate the fever induced by vasopressin in the rat.

The effects of direct administration of vasopressin into the preoptic anterior hypothalamus on thermoregulatory functions were assessed in conscious rats at various ambient temperatures. Intrahypothalamic administration of vasopressin caused fever, increased metabolic heat production and decreased heat loss (cutaneous vasoconstriction) in rats. There was no changes in respiratory evaporative heat loss in response to administration of these drugs. Furthermore, it was found that the fever reactions induced by intrahypothalamic vasopressin was antagonized by pretreatment of animals with an intrahypothalamic dose of either yohimbine (an alpha-adrenergic receptor antagonist), propranolol (a beta-adrenergic receptor antagonist), or sodium acetylsalicylate (a prostaglandin synthetase inhibitor). The data indicate that a prostaglandin-adrenergic link occurs in the hypothalamic pathways which mediate the vasopressin-induced fever in rats.

Animals↗
PubMed1983

Involvement of adrenergic receptor mechanisms within hypothalamus in the fever induced by amphetamine and thyrotropin-releasing hormone in the rat.

The mechanisms underlying the thermal effects induced by intrahypothalamic administration of either d-amphetamine or thyrotropin-releasing hormone (TRH) has been investigated in conscious rats. Direct administration of d-amphetamine (1-10 micrograms in 1 microliter) or TRH (1-4 micrograms in 1 microliter) into the preoptic anterior hypothalamus caused hyperthermia or fever at the ambient temperature (Ta: 8, 22 and 30 degrees C) studied. The fever induced by d-amphetamine or TRH was due to increased metabolic heat production at Ta 8 degrees C, while at Ta 30 degrees C the fever was due to cutaneous vasoconstriction in the rat. At Ta 22 degrees C, the fever was due to both increased metabolism and cutaneous vasoconstriction. Furthermore, the fever induced by intrahypothalamic administration of TRH was greatly reduced by pretreatment with intrahypothalamic administration of either yohimbine (a blocking agent of alpha-adrenergic receptors), phentolamine (a blocking agent of alpha-adrenergic receptors) or DL-propranolol (a blocking agent of beta-adrenergic receptors) in the rat. However, the fever induced by d-amphetamine was antagonized by pretreatment with yohimbine or phentolamine, but not with DL-propranolol in the rat. These observations indicate that the adrenergic receptor mechanisms within the hypothalamus are involved in the fever induced by both d-amphetamine and TRH.

Animals↗
PubMed1983

Effects of anterior pituitary hormones and their releasing hormones on physiological and behavioral functions in rats.

The effects of direct administration of TRH, TSH, LHRH, LH, ACTH, GH, FSH and prolactin into cerebral ventricle system on metabolic, respiratory, cardiovascular and behavioral responses were assessed in unanesthetized rats, Intraventricular administration of TRH, TSH, LHRH or LH caused hypothermia, decreased metabolism and/or cutaneous vasodilation at room temperature (22 degrees C). Intraventricular administration of FSH, ACTH or prolactin caused hyperthermia, increased metabolism and/or cutaneous vasoconstriction. Intraventricular administration of GH caused an insignificant change in thermoregulatory responses. There was no change in respiratory evaporative heat loss in response to either of the drugs tested. In addition, intraventricular administration of TRH, LHRH or LH caused tachycardia, hypertension and a reduction in the epinephrine-induced reflex bradycardia. In contrast, intraventricular administration of prolactin caused bradycardia, hypotension and an enhancement in the epinephrine-induced reflex bradycardia in conscious rats. There was no change in cardiovascular function in response to intraventricular administration of TSH, FSH, ACTH or GH. Furthermore, following intraventricular administration of TRH, but not TSH, LHRH, LH, FSH, GH, ACTH or prolactin three main categories of behavior were provoked: activity of normal type--forward locomotion stimulation, head and body rearing; stereotype activity--increased grooming and head swaying; and abnormal type behavior--tail elevation and piloerection in rats. The data indicate that most of the anterior pituitary hormones and their releasing hormones act through a central mechanism to influence physiological and/or behavioral functions.

Animals↗
PubMed1983

Amino acids injected into the cerebroventricular system induce an enhancement of reflex bradycardia in the rat.

The effects of administration of taurine, GABA and glycine, into the lateral cerebral ventricle, on cardiovascular function were assessed in urethane-anaesthetized rats. Intraventricular administration of either taurine (10-30 micrograms), GABA (5-20 micrograms) or glycine (5-20 micrograms) caused a dose-dependent decrease in both the heart rate and the mean arterial pressure. For example, both the heart rate and the mean arterial pressure fell almost immediately and reached their minimum levels about 5 min after an injection of 20 micrograms of taurine. The cardiovascular responses recovered about 30 min after the injection of taurine. Also, reflex bradycardia was produced in the rats by intravenous infusion of adrenaline (1-5 micrograms/kg). Intraventricular pretreatment of the rats with either taurine, GABA or glycine, although causing no change in the adrenaline-induced pressor effect, did enhance the adrenaline-induced reflex bradycardia. However, pretreatment of the rats intravenously with the same dose of taurine, GABA or glycine had no effect on the adrenaline-induced bradycardia. These data indicate that these amino acids act through a central mechanism to facilitate reflex bradycardia mediated through baroceptor reflexes in response to an acute increase in arterial pressure.

Amino Acids↗
PubMed1983

Involvement of both opiate and catecholaminergic receptors in the behavioural excitation provoked by thyrotropin-releasing hormone: comparisons with amphetamine.

Following direct administration of thyrotropin-releasing hormone (TRH), but not thyroid-stimulating hormone (TSH) or vehicle solution, into the lateral cerebral ventricle in rats, three main categories of behaviour were provoked: activity of the normal type--stimulation of forward locomotion, head and body rearing (as shown by an enhancement in gross movements); stereotyped activity--increased grooming and head swaying (as shown by an enhancement in fine movements); abnormal behaviour--tail elevation and piloerection (as observed grossly). The behavioural excitation caused by TRH was antagonized by pretreatment of the rats with either a narcotic receptor antagonist, naloxone, an alpha-adrenergic receptor antagonists, yohimbine, or a dopaminergic receptor antagonist, haloperidol, but not with a beta-adrenergic receptor antagonist, propranolol. Intraventricular administration of amphetamine to rats caused stimulation of forward locomotion, head and body rearing, increased grooming and sniffing. Unlike TRH, amphetamine did not produce wet-dog shakes, tail elevation and piloerection. Furthermore, the amphetamine-induced excitation was antagonized by pretreatment with a dopaminergic receptor antagonist, haloperidol, but not with either naloxone, yohimbine or propranolol. The data indicate that both opiate and catecholaminergic receptors are involved in the TRH-induced behavioural excitation, whereas dopaminergic receptors are involved in amphetamine-induced excitement in the rat.

Amphetamine↗
PubMed1983

Autonomic dysfunction in palmar hyperhidrosis.

The autonomic (including sudomotor, baroreceptor, and vasomotor) functions were assessed in 3 groups of individuals, comprising 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. Compared with both the normal and hyperhidrotic subjects, the denervated subjects had a much smaller sweating response of both the forehead, the upper chest region and the upper extremities, and a much greater sweating response of both the lateral lumbar and ventral thigh regions in response to body exercise. In addition, cardiovascular responses to either the Valsalva manoeuver, face immersion, or finger immersion were evaluated in these groups of subjects. When compared with those of either the normal or the denervated subjects, the hyperhidrotic subjects had less reflex bradycardia in response to either Valsalva manoeuver or face immersion. In contrast, when compared with those of either the normal or the denervated subjects, the hyperhidrotic subjects had a higher degree of cutaneous vasoconstriction in response to finger (or cold) immersion. The data indicate that the sympathetic fibers passing through the T2-3 ganglia play an important role in the elaboration or modulation of autonomic function elsewhere. Probably, the hyperhidrotic subjects have an over-functioning of the sympathetic nervous fibers which pass through the T2-3 ganglia, which leads to autonomic dysfunction. The autonomic dysfunctions observed in the hyperhidrotic subjects could be eliminated after the interruption of the excessive sympathetic activities passing through the T2-3 ganglia level. A preliminary report of this work was delivered at the 15th Congress of the Pan-Pacific Surgical Association, January 12-18, 1980 and the 12th World Congress of Neurology, September 20-25, 1981.

Adult↗
PubMed1983

Effects of TSH, TRH, LH and LHRH on thermoregulation and food and water intake in the rat.

The effects of administration of thyroid-stimulating hormone (TSH), thyrotropin-releasing hormone (TRH), luteinizing hormone (LH) or luteinizing hormone-releasing hormone (LHRH) into the lateral cerebral ventricle on thermoregulation and food and water intake were assessed in rats. Intracerebroventricular, but not intraperitoneal, injection of TSH, LH or LHRH produced hypothermia in rats at ambient temperatures of both 8 and 22 degrees C. The hypothermia in response to TSH injection was due to both decreased metabolic heat production and increased heat loss (cutaneous vasodilatation). The hypothermia in response to either LH or LHRH was due solely to decreased metabolic heat production. There was no change in respiratory evaporative heat loss in response to TSH, LH or LHRH injection. Furthermore, food but not water intake was greatly reduced following an intracerebroventricular injection of TSH or TRH in rats. On the other hand, intracerebroventricular administration of LH, but not LHRH, caused an increase in relative water intake (or water/food) in rats. However, intracerebroventricular administration of LH or LHRH had an insignificant effect on food intake. The data indicate that, in addition to their hormone actions, TSH, LH and their releasing hormones act through a central mechanism to influence some of the physiological or behavioral functions.

Animals↗
PubMed1982

A dopamine-acetylcholine link in the caudate-putamen complex which mediates metabolic rate.

In order to investigate the possible involvement of the dopaminergic and the cholinergic neurons of caudate-putamen complex (CP) in temperature regulation, we have assessed the effects of administration of either acetylcholine (Ach), atropine (Ach receptor antagonist), apomorphine (DA receptor agonist), or haloperidol (DA receptor antagonist) into the CP on metabolic, respiratory, vasomotor and temperature responses in conscious rats at various ambient temperature (Ta). The results show that intra-CP injection of either Ach or apomorphine caused hypothermia, decreased metabolism and cutaneous vasoconstriction at Ta 8 and 22 degrees C, as well as hyperthermia and cutaneous vasoconstriction at Ta 30 degrees C. On the other hand, intra-Cp injection of either atropine or haloperidol caused hyperthermia, increased metabolism and cutaneous vasoconstriction at all Ta (8, 22, and 30 degrees C) studied. There was no change in respiratory evaporative heat loss in response to these agents at all Ta studied. Furthermore, the Ach-induced hypothermia or hypo-metabolism was antagonized by pretreatment with atropine, but not with haloperidol. However, the apomorphine-induced hypothermia or hypo-metabolism at Ta 8 and 22 degrees C was antagonized by pretreatment with either atropine or haloperidol. These observations tend to indicate that a dopamine-acetylcholine link occurs in the caudate-putamen complex which mediate metabolic rate in the rat.

Acetylcholine↗
PubMed1982

An adrenergic link in the hypothalamic pathways which mediates morphine- and beta-endorphin-induced hyperthermia in the rat.

The mechanism underlying the hyperthermia induced by intrahypothalamic administration of either morphine or beta-endorphin has been investigated in conscious rats. Direct administration of morphine (1--8 micrograms in 1 microliter) or beta-endorphin (1--3 micrograms in 1 microliter) into the anterior hypothalamus caused hyperthermia in rats at the ambient temperature (8, 22 and 30 degrees C) studied. The hyperthermia in response to opiods was brought about by both increased metabolism and cutaneous vasoconstriction. This hyperthermia, unlike the hypothermia induced by intraventricular administration of opiods was not blocked by naloxone nor did tolerance develop to the response. However, the hypothermia induced by intrahypothalamic administration of opioids was greatly reduced by pretreatment with intrahypothalamic administration of either yohimbine (a blocking agent of alpha-adrenergic receptors) or DL-propranolol (a blocking agent of beta-adrenergic receptors) in the rat. These observations suggest that an adrenergic link occurs in the hypothalamic pathways which mediate morphine- and beta-endorphin-induced hyperthermia in the rat.

Animals↗
PubMed1982

Properties of high Q10 units in the conscious duck's hypothalamus responsive to changes of core temperature.

1. Five Pekin ducks were chronically implanted with a device allowing thermal stimulation of the hypothalamus and simultaneous recording of hypothalamic single unit activity on the conscious animals in repeated experiments. In addition, the core temperature of the animals could be lowered by means of a thermode tube which was placed in the colon and was perfused by a cold solution. Hypothalamic temperature was measured in the centre of the hypothalamic thermode array; core temperature was measured in the axillary pit.2. Each unit was tested in two periods of hypothalamic ramp cooling, one was performed at normal core temperature, and the other at a lowered core temperature during sustained intestinal cooling.3. Among forty-six neurones exhibiting a local Q(10) > 2 of their discharge rate, intestinal cooling was found to activate 26% (fall feed-back units), to inhibit 44% (rise feed-back units), and not to affect 30% (non-reactive units). The local Q(10) values of the fall feed-back units were, on average, significantly higher than those of the rise feed-back units.4. By multiple linear regression analysis the thermal coefficients (impulses/sec. degrees C) relating unit discharge to hypothalamic (local) and to core (remote) temperature changes were evaluated. The fall feed-back units exhibited average local temperature coefficients of 0.79+/-0.11 and remote coefficients of -2.75+/-0.56 (means+/-s.e. of mean); the corresponding coefficients of the rise feed-back units were determined as 0.44+/-0.08 and +2.33+/-0.41.5. The results of this study support the hypothesis that the activity of hypothalamic neurones conveying extrahypothalamic cold signals is depressed more by hypothalamic cooling than that of the neurons conveying extrahypothalamic warm signals. This would explain the paradoxical effects of hypothalamic cooling on thermoregulatory effector activity in birds.

Action Potentials↗
PubMed1982

Hypothalamic and striatal dopamine receptor activation inhibits heat production in the rat.

Direct injection of dopaminergic agonist apomorphine into the lateral cerebral ventricle, the preoptic anterior hypothalamus, the caudate-putamen complex, or the globus pallidus caused hypothermia, decreased metabolism and cutaneous vasoconstriction at ambient temperature (Ta) 8 and 22 degrees C, and hyperthermia and cutaneous vasoconstriction in the rat at Ta 30 degrees C. On the other hand, local injection of dopaminergic antagonists such as haloperidol and pimozide into the preoptic anterior hypothalamus and the striatal nuclei caused hyperthermia, increased metabolism and cutaneous vasoconstriction at Ta 8, 22, and 30 degrees C. However, there was no change in respiratory evaporative heat loss in response to administration of either dopaminergic agonist or antagonists in the rat at all Ta studied. The data indicate that hypothalamic and striatal dopaminergic receptor activation inhibits metabolic heat production in rats. In addition, intrahypothalamic injection of 5-hydroxytryptamine caused hypothermia, decreased metabolism and cutaneous vasodilatation in the rat at Ta 8 and 22 degrees C, whereas at Ta 30 degrees C caused an insignificant change in the thermoregulatory responses. Furthermore, the thermal responses induced by intrahypothalamic injection of apomorphine were not altered by depletion of hypothalamic 5-hydroxytryptamine. These observations do not support the contention that there is a dopamineserotonin link in the hypothalamic pathways that mediate heat loss mechanisms in the rat.

5,7-Dihydroxytryptamine↗
PubMed1982

Effects of intracerebroventricular administration of thyrotrophic-releasing hormone on cardiovascular function in the rat.

The effects of administration of thyrotrophic-releasing hormone (TRH) into the lateral cerebral ventricle on cardiovascular functions were assessed in both urethane-anesthetized and unanesthetized rats. Intracerebroventricular administration of TRH (10-60 micrograms in 5.0 microliters volume) caused a dose-dependent increase in both the heart rate and the mean arterial pressure. For example, both the heart rate and the arterial pressure rose almost immediately and reached their maximal levels about 4 min after an injection of 40 micrograms TRH. The cardiovascular responses recovered about 10 min after the TRH injection. In addition, reflex bradycardia was produced by intravenous infusion of epinephrine (1.0-5.0 micrograms/kg) in rats. Over the dose range of epinephrine used, a dose-dependent bradycardia was obtained. It was found that intracerebroventricular pretreatment of animals with TRH, although causing no change in the epinephrine-induced pressor effect, did reduce the epinephrine-induced reflex bradycardia in rats. However, intravenous pretreatment of animals with the same dose of TRH had no effect on the epinephrine-induced bradycardia. Thus, the data indicate that TRH acts through a central mechanism to inhibit reflex bradycardia mediated through baroreceptor reflexes in response to acute increase in blood pressure.

Animals↗
PubMed1982

Activation of dopaminergic receptors within the caudate-putamen complex facilitates reflex bradycardia in the rat.

The cardiovascular responses to intravenous doses of epinephrine were assessed in sham-operated, substantia nigra (SN)-lesioned, and SN-stimulated rats under urethane anesthesia. Activation of nigrostriatal dopamine pathways with SN stimulation, although showing no alteration in the epinephrine-induced hypertension, did produce a significant enhancement in reflex bradycardia compared to the controls. In contrast, inhibiting nigrostriatal dopamine pathways with SN lesions led to a significant reduction in the epinephrine-induced bradycardia. Furthermore, local injection of a dopamine receptor agonist apomorphine into the caudate-putamen complex (CP) facilitated reflex bradycardia, while intra-CP injection of dopamine antagonists such as haloperidol and pimozide inhibited it. Moreover, the enhancement in the reflex bradycardia induced by intra-CP administration of apomorphine could readily be abolished by pretreatment with intra-CP administration of either haloperidol or pimozide. Therefore, the present data indicate that a dopaminergic synapse occurs within the caudate-putamen complex which mediates reflex bradycardia in the rat.

Animals↗
PubMed1982

A norepinephrine-cyclic AMP link in the hypothalamic pathways which mediate fever induced by endotoxin and prostaglandin E2 in the rat.

The changes in rectal temperature, metabolic rate, cutaneous temperatures and respiratory evaporative heat loss produced by an injection of a bacterial endotoxin piromen (4-40 ng in 1 microliter) into the anterior hypothalamus were assessed in conscious rats in both sexes from a wide range of body mass and at various ambient temperatures (TaS). Intrahypothalamic injection of piromen increased metabolism and decreased cutaneous temperatures which led to fever in rats at Ta 8-30 degrees C. The monophasic fever was not significantly correlated with either body mass, sex difference of the Ta at which the experiments are carried out. Furthermore, daily intrahypothalamic injections of piromen produced no pyrogenic tolerance. Intrahypothalamic injections of either prostaglandin E2, norepinephrine, aminophylline or dibutyryl cyclic AMP also produced increased metabolism and decreased cutaneous temperature which led to fever at Ta 8-30 degrees C. In addition, the fever induced by intrahypothalamic injections of piromen, prostaglandin E2 or nor-epinephrine was greatly antagonized by pretreatment with intrahypothalamic injections of alpha or beta adrenergic antagonist. However, the fever induced by dibutyryl cyclic AMP or aminophylline was not affected by pretreatment with adrenergic receptor blockade. The data indicate that a norepinephrine- cyclic AMP link occurs in the hypothalamic pathways which mediate the piromen-induced or the prostaglandin E2-induced fever in rats.

Aminophylline↗
PubMed1981

Effects of intracerebroventricular injection of clonidine on metabolic, respiratory, vasomotor and temperature responses in the rabbit.

1. The thermoregulatory outputs (including metabolic, respiratory and vasomotor activities) produced by an injection of clonidine or 5-hydroxytryptamine (5-HT) into the third cerebral ventricle of conscious rabbits were assessed at three different ambient temperatures (Ta) of 2, 22 and 32 degrees C. 2. When injected into the third cerebral ventricle, both clonidine and 5-HT produced a dose-dependent hypothermia in rabbits at both 2 and 22 degrees C Ta. The hypothermia was due to a decrease in metabolic heat production (M) at 2 degrees C Ta, while at 22 degrees C Ta the hypothermia was due to cutaneous vasodilatation. There were no changes in respiratory evaporative heat loss. 3. Furthermore, the clonidine-induced hypothermia was greatly reduced by pretreatment of the animals with either 5,6-dihydroxytryptamine (impairment of central 5-HT pathways) or yohimbine (alpha-adrenergic blocking agent), but not by 6-hydroxydopamine (impairment of central catecholamine pathways). 4. The results indicate that clonidine may act on the alpha-adrenergic receptors located on central 5-HT pathways to produce a hypothermic action by promoting a decrease in heat production or an increase in heat loss in the rabbit.

5,6-Dihydroxytryptamine↗