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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine winter swimmer men were exposed to: (A) sauna and ice water immersion; (B) sauna and 15 degrees C shower; (C) sauna and room temperature; (D) head-out ice-water immersion and room temperature. The exposures were repeated and ended with a recumbent recovery. The initial, post-exposure and post-recovery concentrations of plasma ACTH, serum cortisol, serum melatonin, plasma norepinephrine and plasma epinephrine were determined. ACTH and cortisol indicated a slightly increased post-exposure level. Melatonin concentration did not change. Post-exposure norepinephrine levels increased (P less than 0.05) from the initial. Post-exposure epinephrine indicated a tendency to elevated levels with a nearly doubled (P less than 0.05) concentration in experiment A. The tendency toward enhanced ACTH and cortisol secretion and sympathetic activity shown by increased catecholamine secretion suggest that the winter swimming practice may raise the pain threshold and develop a potential for improved cold tolerance, possibly by nonshivering thermogenesis.
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PMID:Some endocrine responses to sauna, shower and ice water immersion. 278 70

This study was undertaken to determine the secretion of aldosterone by male Long-Evans rats acclimated for six weeks to moderate cold (15 C), in comparison with rats maintained at thermo-neutral temperature (28 C). The following determinations were made: corticosteroids in plasma and adrenals, PRA, and hydromineral balance. Cold acclimation highly increased the plasma and adrenal levels of aldosterone and corticosterone. The cold stimulation of aldosterone was induced neither by the renin-angiotensin system, nor by alterations of hydromineral balance: PRA, plasma sodium and potassium concentrations, blood hematocrit, and hydromineral balance at 15 C and 28 C did not differ. Moreover this stimulation was induced neither by ACTH, nor by any other hypophyseal factors, since plasma aldosterone levels remained high in hypophysectomized rats. This study provides evidence of an aldosterone stimulation which appeared during moderate cold acclimation; the origin of this stimulation must be investigated.
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PMID:Evidence for a cold-induced aldosterone stimulation in the rat. 281 57

A 71-year-old man was referred to Tokai University Hospital because of cold intolerance, slow speech and slowing down of his intellectual and motor activities. Free thyroxine index, and free T-4 and T-3 levels were low (1.4, 0.7 ng/dl and 0.4 ng/ml, respectively) with normal TSH (2.5 microIU/ml). A skull X-ray showed enlargement of the sella turcica and his CT scan revealed an intrasellar mass. LH, FSH, ACTH and PRL did not rise in response to the intravenous administration of LH-RH and insulin. A diagnosis of pan-hypopituitarism due to a pituitary tumor was established. The release of ACTH and cortisol was restored under stimulation of CRF or lysine vasopressin. TSH responded to TRH in a delayed manner. The pituitary tumor was removed by a transsphenoidal operation and diagnosed histologically as craniopharyngioma. Our hospital has experienced nine cases of craniopharyngioma in the last 10 years but the present case was the only intrasellar craniopharyngioma.
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PMID:A case of intrasellar craniopharyngioma. 283 33

The effects of cyclosporine on the adrenocortical stress response in Wistar male rats were examined. The adrenocortical response to cold exposure as assessed by serum corticosterone levels was suppressed significantly (25.2%) following the oral administration of 10 mg/kg/day cyclosporine for 10 days compared to that of controls (p less than 0.05). Stress response to cold exposure was also suppressed significantly to a greater extent in rats coadministered with cyclosporine plus 1 or 4 mg/kg/day of prednisolone than in rats administered with each dose of prednisolone alone (16.8% greater for 1 mg/kg prednisolone group; p less than 0.01, or 22.3% greater for 1 mg/kg prednisolone group; p less than 0.005). Stress response of ACTH was also suppressed significantly to a greater extent in animals coadministered with cyclosporine plus 1 or 4 mg/kg/day of prednisolone than in rats administered with each dose of prednisolone alone (37.5% greater for 1 mg/kg prednisolone group; p less than 0.025, or 25.7% greater for 4 mg/kg prednisolone group; p less than 0.025). However, the decrement in ACTH levels by cyclosporine did not always result in corresponding decrement of serum corticosterone levels. These results suggest that cyclosporine decreases the adrenocortical response in part via suppression of the pituitary-adrenal axis. However, direct effects of cyclosporine on the adrenal gland should not be neglected.
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PMID:Effects of cyclosporine on adrenocortical stress response of Wistar rats. 283 19

The method of intestinal cooling was used to analyze the effect of centrally administered ACTH in microgram quantities on hypothalamic centers regulating activity of thermoregulatory outputs (cold thermogenesis--CT, peripheral vasomotor tone--PVMT, respiratory evaporative heat loss--REHL). ACTH, when injected into the supraoptic area of the anterior hypothalamus of normal rabbits, had no significant effect on body temperature control. Intrahypothalamic administration of ACTH during the early phase of the fever, induced by intravenous injection of exogenous pyrogen, evoked dissociation of temperature thresholds for cold and warm defence, shifting the threshold for induction of cold thermogenesis to lower central temperatures. The thermosensitivity of centers controlling cold thermogenesis was lowered and the maximal values of cold thermogenesis were depressed to about 30% of those in control rabbits. Central administration of ACTH in the late phase of the fever (120 min after IV injection of endotoxin) induced a smaller effect than in the early phase of the fever--the downward shift of the temperature threshold for cold thermogenesis was less evident and the thermosensitivity of the controller remained unchanged. The changes in activity of thermoregulatory centers that occurred after ACTH in febrile rabbits correspond to those observed in the late phase of the fever in ACTH-untreated rabbits. It is suggested therefore, that the presumed increase in ACTH production during fever might represent a negative feed-back mechanism contributing to the termination of the febrile state.
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PMID:Mode of ACTH antipyretic action. 285 94

A child is reported with adrenocortical unresponsiveness to ACTH and autonomic dysfunction. The latter consisted of cold extremities, progressive loss of tear production, the development of achalasia of the esophagus, pupillary dysfunction, and an abnormal histamine skin test. These findings suggest progressive parasympathetic denervation as a cause for the adrenocortical abnormality.
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PMID:Autonomic dysfunction and adrenocortical unresponsiveness to ACTH. 285 Mar 14

ACTH peptides influence the developing nervous system during the first three weeks of life in the rat. ACTH 4-10 and Org 2766 (10.0 micrograms/kg) accelerate the expression of motor hyperactivity usually exhibited in 15-day old normal animals, with ACTH 4-10 increasing the force of extensor digitorum longus muscle contraction amplitude. Following cold stress and peptide treatment, rate changes in motor activity from one age to the next are dramatically enhanced, with vertical activity being exhibited at an earlier age than controls. Grasping ability is similarly enhanced in 13-day old ACTH 4-10-treated animals. The retention of a T-maze learning paradigm is significantly enhanced in 16-day old ACTH 4-10 (10.0 micrograms/kg)-treated and Org 2766 (0.01 micrograms/kg)-treated animals, with these animals running the maze significantly faster than controls. Peptide treatment appears to reverse the apparent turning preference in the maze during extinction. It is suggested that ACTH peptides modulate the organization of the nervous system and facilitate neurotransmission, and may act on dopaminergic and cholinergic neurotransmitter systems. Motor behavior seems to reflect underlying neural substrates that are integrated to produce the overt behavior of the organism.
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PMID:ACTH neuromodulation of the developing motor system and neonatal learning in the rat. 286 32

1. Pigeon brain acetone powder was extracted with a mixture of acetone, water and hydrochloric acid (40:21:1 v/v/v). The extract was added to a large volume of chilled acetone. 2. The resultant precipitate was washed with cold acetone and then chromatographed on Sephadex G-25. The void volume peak constituted fraction A. The trailing peak immediately following fraction A was divided into two fractions designated B and C. 3. Fraction B (mol. wt less than 5,000) stimulated corticosterone production in isolated rat adrenal cells while the other fractions were devoid of similar ACTH-like bioactivity. 4. None of the fractions showed activity in the opiate radioreceptor assay or hot plate test, implying the absence or presence of only trace amounts of opiate-like materials. Other possibilities that cannot be ruled out include the presence of molecules with substitutions in the sequence by amino acids that result in little or no activity.
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PMID:Corticotropin-like material in pigeon brains. 288 94

Adrenocortical function and the intensity of lipid peroxidation in the liver of animals fed the diet containing alpha-tocopherol (4 mg/day/rat for 7 days) and exposed to cold stress for 2, 5 and 20 hours were studied in vitro. It was established that alpha-tocopherol reduces the duration of the corticosterone secretion augmentation under cold stress but raises the sensitivity of the adrenals to ACTH. The action of the antioxidant correlated with its content in the tissues and inhibition of the cold-induced activation of lipid peroxidation.
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PMID:[Effect of alpha-tocopherol on the adrenal reaction to cold stress]. 299 Jun

Ether-laparotomy stress produced a rapid increase in rat hypothalamic CRF concentration, followed by a rapid reduction and subsequent increase. Cold-restraint stress significantly reduced hypothalamic CRF concentration at 15 min after stress onset. Serum ACTH and corticosterone levels were significantly elevated at 15 min after the onset of both stresses. The CRF responses in the medulla oblongata were not similar to the hypothalamic CRF responses. Norepinephrine concentration in the hypothalamus was reduced, whereas dopamine concentration in the hypothalamus and medulla oblongata was significantly increased. Epinephrine concentrations in these tissues did not show any significant change throughout the stress period. The observations lead to the following conclusions: hypothalamic CRF plays a major role in stimulating ACTH secretion under acute stress; the reduction in hypothalamic CRF is due to an excess release in the early phase of acute stress; hypothalamic CRF and medulla oblongata CRF are controlled by different mechanisms; norepinephrine in the hypothalamus may not be involved in stimulating hypothalamic CRF secretion in the early phase of acute stress; and catecholamines are regulated differently in the hypothalamus and medulla oblongata.
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PMID:Brain corticotropin-releasing factor (CRF) and catecholamine responses in acutely stressed rats. 300 28


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