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Biomedical subjects

L R Shian

Publications and source records attributed to L R Shian.

36 records · Page 2Linked to original sources
PubMed1985

Effects of cholecystokinin octapeptide on thermoregulatory responses and hypothalamic neuronal activity in the rat.

Rats were chronically implanted with a hypothalamic cannula to allow chemical stimulation of the hypothalamus on the conscious animals in repeated experiments. Direct administration of cholecystokinin octapeptide (CCK-8) (20-60 ng) into the preoptic anterior hypothalamic area caused a dose-related fall in rectal temperature at ambient temperatures of 8 degrees C and 22 degrees C. The hypothermia induced by CCK-8 was produced by a decrease in metabolism at an ambient temperature of 8 degrees C, whereas at 22 degrees C, it was caused by both a decrease in metabolism and an increase in cutaneous temperature. However, at an ambient temperature of 30 degrees C, intrahypothalamic administration of CCK-8 caused an insignificant change in thermoregulatory responses. Furthermore, neither intrahypothalamic injection of 0.9% saline nor intraperitoneal injection of CCK-8 (60 ng) had any effect on thermoregulatory responses at the ambient temperatures of 8 degrees-30 degrees C studied. Under urethane anaesthesia, 59 single neurons in the preoptic anterior hypothalamic area were examined in 29 rats. Each animal was subjected to scrotal warming or cooling and to the administration of CCK-8. Microiontophoretic application of CCK-8 resulted in inhibition of the majority (75%) of cold-responsive neurons as well as excitation of the majority (77.8%) of warm-responsive neurons recorded in the preoptic anterior hypothalamic area. However, the majority (69%) of thermally unresponsive cells were not affected by CCK-8 application. The data indicate that CCK-8, when administered intrahypothalamically, excites warm-responsive neurons and inhibits cold-responsive neurons within the preoptic anterior hypothalamic area to induce hypothermia by promoting an increase in heat loss and a decrease in heat production.

Animals↗
PubMed1985

Thyrotropin-releasing hormone-induced hyperglycemia: possible involvement of cholinergic receptors in the lateral hypothalamus.

The influence of the site of action of thyrotropin-releasing hormone (TRH) on the production of hyperglycemia was studied in rats by comparing the effectiveness of TRH administered by different routes. Administration of TRH (5 micrograms) into the lateral hypothalamus (LH) produced a hyperglycemia with a peak elevation of blood glucose of 140 mg/dl. Injection of 5 micrograms TRH into the ventromedial hypothalamus (VMH) produced a blood glucose elevation of 44 mg/dl, while injection of the same dose of TRH into the anterior hypothalamus (AH) produced a blood glucose elevation of 23 mg/dl. These findings indicate an LH site of action of TRH. Indeed, intra-LH administration of TRH (1-10 micrograms) caused dose-related increases in blood glucose. Administration of acetylcholine into the same site was also shown to induce hyperglycemia. The hyperglycemic effects of TRH and acetylcholine were antagonized by previous treatment of the LH site with atropine, a cholinergic receptor antagonist. Furthermore, the TRH-induced hyperglycemia was not observed or was greatly reduced in spinal rats or in adrenalectomized rats. The results indicate that TRH may act through the cholinergic receptor mechanisms within the LH region to induce hyperglycemia by promoting an increase in the sympathetic-adrenal medullary efferent activity.

Acetylcholine↗
PubMed1985

Hypothalamic involvement in the locomotor stimulant or satiety action of thyrotropin-releasing hormone and amphetamine.

To determine whether the locomotor stimulant and the anorexic actions of thyrotropin-releasing hormone (TRH) and amphetamine were mediated through the hypothalamic nuclei, rats were infused with either TRH or amphetamine through previously implanted hypothalamic cannulae. Administration of TRH or amphetamine into the ventromedial hypothalamus, but not the lateral hypothalamus and the anterior hypothalamus, caused locomotor stimulation in rats. On the other hand, administration of TRH or amphetamine into the lateral hypothalamus, but not the ventromedial hypothalamus or the anterior hypothalamus, caused a reduction in food consumption without affecting relative water intake (or water-to-food ratio) in the rat. The data indicate that the ventromedial hypothalamus is the most sensitive site of the TRH- or amphetamine-induced locomotor stimulation and the action of TRH or amphetamine on the lateral hypothalamus is also a possible mechanism mediating anorexia.

Amphetamine↗
PubMed1985

Long term treatment of Graves' hyperthyroidism with sodium ipodate.

To investigate the long term usefulness of sodium ipodate (Oragrafin) in the management of Graves' hyperthyroidism, we studied the effects of ipodate (500 mg, orally, daily for 23-31 weeks) on serum T3, T4, rT3, and some clinical parameters in five newly diagnosed Graves' hyperthyroid patients. Mean pretreatment serum T3, T4, and rT3 concentrations were 780 ng/dl, 25.4 micrograms/dl, and 118 ng/dl, respectively. One day after the first dose of ipodate, serum T3 decreased by 62% (P less than 0.01), and it was within the normal range thereafter throughout treatment. The serum T4 concentration decreased by 20% (P = 0.09) at 24 h and by 43% (P less than 0.05) at 14 days. Subsequently, serum T4 was 41-65% lower than before treatment throughout the study; rT3 increased 24 h after the first dose of ipodate (118% above baseline; P = 0.1), remained elevated (97-109%) for 10 weeks, and then gradually decreased to the pretreatment level. A marked gain in body weight [5.1 +/- 1.1 (+/- SEM) kg] occurred in all patients. After discontinuation of ipodate, mean thyroid radioiodine (RAI) uptake values increased serially in four patients and were similar to pretreatment values: pretreatment, 74 +/- 6% (+/- SEM); after 7 days, 66 +/- 8%; after 14 days, 71 +/- 7%; after 28 days, 69 +/- 7%. The fifth patients's RAI uptake was 12-16% (vs. a pretreatment value of 48%) from 7-28 days after the end of a 31-week course of ipodate. He remained euthyroid without further treatment for the subsequent 4 months. We conclude that 1) ipodate (500 mg daily) reduces serum T4 and T3 levels as fast and as much as does the 1-g daily dose studied previously; 2) long term use (for 23-31 weeks) of ipodate for the treatment of Graves' hyperthyroidism is clinically feasible; no adverse effects occurred during or after ipodate treatment; and 3) RAI uptake returns to pretreatment levels as early as 7 days after the discontinuation of ipodate. Hence, use of ipodate does not prevent use of 131I therapy for those patients for whom it is otherwise desirable.

Adult↗
PubMed1984

Effects of hypothalamic noradrenaline depletion with 6-hydroxydopamine on the body temperature regulation of the rat.

Rats which had been pretreated with 3 intrahypothalamic doses of 10 micrograms of 6-hydroxydopamine (6-OHDA) to cause a selective depletion of hypothalamic noradrenaline to 26.7% of control hypothalamic noradrenaline maintained rectal temperature within the normal limits displayed by the control group. However, noradrenaline-depleted rats displayed a decrease in both cutaneous temperature and metabolic heat production in the cold (8 degrees C). Intrahypothalamic injections of 6-OHDA in normal rats at room temperature (22 degrees C) caused an acute hyperthermia of up to 1.1 degree C which lasted for about 6 h. The acute hyperthermia in response to 6-OHDA was due to both cutaneous vasoconstriction and increased metabolism in the rat. Selective depletion of hypothalamic noradrenaline without affecting hypothalamic dopamine by prior treatment with 6-OHDA markedly reduced the hyperthermic responses to a subsequent dose of 6-OHDA. Therefore, the acute hyperthermic responses to 6-OHDA may be related to a release of noradrenaline in the hypothalamus. The data indicate that activation of noradrenergic pathways in the hypothalamus facilities heat production and inhibits heat loss mechanisms in the rat.

Animals↗
PubMed1984

Clonidine-induced hypothermia: possible involvement of cholinergic and serotonergic mechanisms.

The thermoregulatory effects (including metabolic, vasomotor and respiratory activities) produced by an injection of clonidine (1-3 micrograms in 0.5 microliter) into the preoptic anterior hypothalamus were assessed in conscious rats at ambient temperatures (Ta) of 8, 22 and 30 degrees C. Intrahypothalamic administration of clonidine caused a dose-dependent fall in rectal temperature at Ta 8 degrees C and 22 degrees C. The hypothermia in response to clonidine was due to decreased metabolic heat production and/or cutaneous vasodilation. There was no change in respiratory evaporative heat loss. The clonidine-induced hypothermic response was attenuated by pretreatment of the rats with either 5,7-dihydroxytryptamine (10 micrograms, administered intrahypothalamicly, 14 days before clonidine injection), yohimbine (0.2 microgram, administered intrahypothalamicly, 10 min before clonidine injection), cyproheptadine (1 microgram, administered intrahypothalamicly, 10 min before clonidine injection), or atropine (0.1 microgram, administered intrahypothalamicly, 10 min before clonidine injection). The data indicate that clonidine may act on alpha-adrenoceptors located on a serotonin-acetylcholine pathway within the preoptic anterior hypothalamus to induce hypothermia by promoting a reduction in metabolic heat production and/or an enhancement in dry heat loss in rats.

5,7-Dihydroxytryptamine↗
PubMed1981

Adrenal influence on pituitary secretion of thyrotropin and prolactin in rats.

Basel plasma levels and pituitary content of TSH and PRL were measured in young male rats after bilateral adrenalectomy with and without corticosterone replacement. Adrenal ablation for a period of 4 days resulted in the arrest of body weight gain, a remarkable hemoconcentration, the slight and insignificant increase in plasma TSH and PRL, but no significant changes in the pituitary content of TSH and PRL and the hypothalamic content of catecholamines, as compared with the control animals. Adequate glucocorticoid replacement in adrenalectomized rats, as determined by the plasma level of corticosterone, did not result in a comparable weight gain, as in the control group, but did reduce plasma protein to almost normal levels. The plasma levels of TSH and PRL in the adrenalectomized animals were significantly suppressed, although the pituitary contents of TSH and PRL were not different from the control values. Four days after adrenalectomy, pituitary stimulation tests with TRH, chlorpromazine, and metoclopramide produced much higher levels of plasma TSH and PRL in the adrenalectomized rats than in the control group. Replacement of corticosterone in the adrenalectomized rats diminished the excess of TSH and PRL responsiveness. These results suggest that adrenal glands may not be directly involved in the hypothalamic control of the pituitary content of TSH and PRL, as they are in the case of ACTH. However, physiological levels of glucocorticoids clearly exert an inhibitory effect on TSH and PRL release by the pituitary gland in response to provocative stimulation.

Adrenal Glands↗
PubMed1981

A serotonergic mechanism of the prolactin-stimulating action of metoclopramide.

The PRL-stimulating effect of metoclopramide (2-methoxy-5-chloroprocainamide) was examined in normal and adrenalectomized male rats pretreated with DL-p-chlorophenylalanine methyl ester (PCPA), an inhibitor of serotonin biosynthesis. PCPA significantly reduced the hypothalamic content of serotonin, increased basal PRL in adrenalectomized rats but not in controls, and potentiated PRL elevation in response to metoclopramide. In the PCPA-pretreated groups, the maximal PRL response to metoclopramide was 60% and 85% higher than that in the saline controls of normal and adrenalectomized rats, respectively. PCPA did not enhance the PRL-stimulating effect of haloperidol, a well established dopamine antagonist, L-alpha-Methyl-p-tyrosine pretreatment in rats depleted hypothalamic dopamine without any change in serotonin and elevated basal PRL, but failed to show an additive effect with metoclopramide's action on serum PRL. Rats pretreated with mianserin, a specific brain serotonin receptor blocker, attenuated PRL elevation in response to low doses of metoclopramide but produced the same response to high doses of metoclopramide as the control rats. These data indicated that metoclopramide stimulated rats pituitary PRL secretion by a serotonergic mechanism in addition to its dopamine antagonist properties.

Adrenalectomy↗
PubMedDate not supplied

Correlation between plasma cortisol and CSF catecholamines in endogenous depressed dexamethasone nonsuppressors.

Nineteen endogenous depressive in-patients (13 with major depression and 6 with bipolar disorder-depressed) and 10 other patients with dysthymic disorder serving as the control group were given the dexamethasone suppression test (DST, 1 mg/subject). The results showed that the DST sensitivity in endogenous depressives was 73.7% and the specificity was 90%. After the patients were treated daily for 6 weeks with 150-200 mg imipramine, 88.9% of those endogenous depressive patients who previously had a positive DST response exhibited a negative response. Moreover, a significantly negative correlation was found between the CSF norepinephrine level and the pre-dexamethasone 4 p.m. plasma cortisol level in those endogenous depressed patients who had a positive DST response. Pre-treatment data also showed that the 4 p.m. plasma cortisol had a significant negative correlation with CSF dopamine. These findings suggest that endogenous depression with positive DST could be related not only to a lower norepinephrine level, but also to a lower dopamine level.

Adult↗