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Biomedical subjects

A Chandra

Publications and source records attributed to A Chandra.

At least 145 records · Page 8Linked to original sources
PubMed1981

Needle stimulation of acupuncture loci Chu-Chih (LI-11) and Ho-Ku (LI-4) induces hypothermia effects and analgesia in normal adults.

The effects of acupuncture stimulation on the Chu-Chih (LI-11) and Ho-Ku (LI-4) loci on both thermoregulatory function and analgesic activity were assessed in normal adults. Stimulation of Chu-Chih and Ho-Ku each produced both hypothermia and analgesia. The hypothermia was brought about by decreased metabolic heat production and cutaneous vasodilatation (as estimated by an increase in cutaneous temperature). The analgesic effect was shown by an increase in the latency to palm lift in the hot plate test. Thus, the data indicate that stimulation of acupuncture loci Chu-Chih and Ho-Ku is an ideal treatment for both the fever and painful syndromes.

Acupuncture Therapy↗
PubMed1981

Serotoninergic mechanisms of the hypothermia induced by clerodenron fragrans (Ventenaceae) in the rat.

The effects of the Chinese herb Chou-Mou-Li, clerodenron fragrans (Ventenaceae) on metabolic, respiratory and vasomotor activities as well as body temperature were assessed in conscious rats at three different ambient temperatures (Ta) of 8, 22 and 30 degrees C. Intraperitoneal administration of Chou-Mou-li produced dose-dependent hypothermia in rats at both 8 and 22 degrees C Ta- At 8 degrees C Ta the hypothermia in response to Chou-Mou-Li was due to decreased metabolism, while at 22 degrees C Ta the hypothermia was due to both decreased metabolism and cutaneous vasodilatation. There was no change in respiratory evaporative heat loss. Furthermore, the hypothermia induced by Chou-Mou-Li was greatly antagonized by pretreatment of animals with p-chlorophenylalanine (a selective depletor of brain serotonin), but not by either atropine sulfate (a selective blocker of cholinergic receptors), regitine (a selective blocker of alpha-adrenergic receptors) or DL-propranolol (a selective blocker of beta-adrenergic receptors). However, at 30 degrees C Ta, systemic administration of Chou-Mou-Li produced no change in rectal temperature or other thermoregulatory responses. On the other hand, direct administration of serotonin into the lateral cerebral ventricle of conscious rats also produced dose-dependent hypothermia at 8 and 22 degrees C Ta. Again, the hypothermia in response to serotonin was due to decreased metabolism at 8 degrees C Ta and was due to both decreased metabolism and cutaneous vasodilatation at 22 degrees C Ta. At 30 degrees C Ta administration of serotonin also produced no change in thermoregulatory functions. The data indicate that Chou-Mou-Li produces hypothermia by increasing sensible heat loss and decreasing metabolic heat production, probably via the release of endogenous serotonin within brain.

Animals↗
PubMed1981

Effects of needle stimulation of acupuncture loci Nei-Kuan (EH-6), Tsu-San-Li (St-36), San-Yin-Chiao (Sp-6) and Chu-Chih (LI-11) on cutaneous temperature and pain threshold in normal adults.

The effects of stimulation of acupuncture loci Nei-Kuan (EH-6), Tsu-San-Li (St-36), San-Yin-Chiao (Sp-6) and Chu-Chih (LI-11) on cutaneous circulation and/or pain threshold were assessed in eight normal adults. Stimulation of acupuncture locus San-Yin-Chiao (located in the right leg) produced vasoconstriction in the right leg skin temperature (Tright leg) and in the left leg skin temperature (Tleft leg). There was no change in either right arm skin temperature (Tright arm), left arm skin temperature (Tleft arm), metabolic rate, or respiratory evaporative heat loss. Stimulation of Nei-Kuan (located in the right arm) produced vasoconstriction only in both Tright arm and Tleft arm without changes in Tright leg or Tleft leg. Stimulation of acupuncture locus Tsu-San-Li (located in the left leg) produced vasoconstriction in both Tleft leg and Tright leg without changes in either Tright arm or Tleft arm. Stimulation of acupuncture locus Chu-Chih (located in the left arm) produced vasodilatation in both Tleft arm and Tright arm without changes in either Tright leg or Tleft leg. On the other hand, stimulation of acupuncture locus San-Yin-Chiao (right side) produced analgesia only in the right foot sole, while stimulation of acupuncture locus Chu-Chih (left side) produced analgesia only in the left hand palm. Thus, the data indicate that each acupuncture locus may have its own topographical representation with special reference to both cutaneous circulation and pain threshold in normal adults.

Acupuncture Therapy↗
PubMed1980

Effects of thyrotrophic-releasing hormone (TRH) on thermoregulation in the rat.

At ambient temperatures (Ta) of both 8 and 22 degrees C, intraventricular administration of TRH (10-80 microgram) produced a dose-dependent hypothermia in rats. The hypothermia was due to both decreased metabolic heat production and cutaneous vasodilatation. In contrast, at 30 degrees C Ta, TRH increased metabolic heat production (due to behavioral excitation) and led to hyperthermia.

Animals↗
PubMed1980

Intraventricular administration of isoproterenol inhibits both heat production and heat loss mechanisms in rats.

At an ambient temperature (Ta) of 8 degrees C, intraventricular administration of isoproterenol inhibited metabolic heat production and led to hypothermia in rats. In contrast, at a Ta of 22 degrees C and of 30 degrees C, isoproterenol decreased cutaneous circulation and led to hyperthermia. The data indicate that isoproterenol inhibits both heat production and heat loss mechanisms in rats.

Animals↗
PubMed1980

Transplacental infection with Japanese encephalitis virus.

During a widespread epidemic of Japanese encephalitis, five pregnant women affected by the illness were observed. The diagnosis of Japanese encephalitis virus (JEV) infection was established on the basis of clinical presentation, rising titers of hemagglutination-inhibiting antibody, and the presence of specific IgM antibodies. Two women aborted, two were delivered of apparently normal children, and the fate of one case is not known. From brain, liver, and placental tissues of one of the aborted fetuses, JEV was isolated. This appears to be the first report of human transplacental infection with JEV.

Adult↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1980

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↗
PubMed1979

Effects of gamma-hydroxybutyric acid on metabolic, respiratory and vasomotor activities and body temperature in rats.

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.

Animals↗