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

Total body water, water intake, urine output, milk yield, plasma, milk and urine osmolality and plasma arginine vasopressin concentration were measured in goats exposed to thermoneutral (20 degrees C) and cold (0-1.0 degrees C) environments for 24 h. Cold exposure caused the animals to reduce their water intake substantially. This was accompanied by a decrease in total body water and an increase in osmolality of plasma and milk. The output of urine decreased as cold exposure progressed but free water clearance by the kidney was not significantly different in thermoneutral and cold environments and cold exposure had no effect on circulating arginine vasopressin concentration. Milk yield was reduced by cold exposure and it is suggested that the reduced net movement of water from blood to milk is partly a consequence of the dehydration induced by cold exposure and that this, in turn, is due primarily to a decrease in water intake with no effective renal compensation.
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PMID:The effect of cold exposure on fluid balance, circulating arginine vasopressin concentration and milk secretion in the goat. 719 Jun 79

The effects of hemorrhage on the febrile response of the sheep was examined because hemorrhage is a potent stimulant for arginine vasopressin (AVP) release into cerebrospinal fluid and blood. Removal of 20% of the estimated blood volume of the conscious sheep led to small physiologic changes and significantly decreased fevers in response to bacterial endotoxin. Mean arterial blood pressure decreased in hemorrhaged febrile sheep to a significantly greater extent than in nonhemorrhaged febrile sheep. AVP levels were considerably greater in the blood of hemorrhaged febrile sheep than in nonhemorrhaged febrile sheep and the concentrations correlated with the magnitude of the decrease in fever. Sheep hemorrhaged in the cold had changes in body temperature similar to control sheep. These experiments support the hypothesis that AVP may be an antipyretic neuromodulator.
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PMID:Effect of hemorrhage on fever: the putative role of vasopressin. 723 49

To assess the ability of the liver to remove immunoreactive arginine vasopressin (AVP) from the circulation and to determine the effect of certain metabolic factors on the process, a study was carried out with rat livers perfused at 37 C with an oxygenated albumin--electrolyte solution containing AVP (117 +/- 4.5 muU/ml). In controls, the hepatic clearance of AVP was 795 +/- 120 microliter/min (SEM). The addition of AVP in concentrations up to 9029 microU/ml, perfusion with a glucose-free medium, or perfusion without oxygen did not significantly alter the hepatic clearance of AVP. However, perfusion with cold medium (11 C) significantly altered AVP removal in that initially AVP removal increased, while later on AVP removal became completely inhibited. This phenomenon may possibly be a consequence of a cold-induced increase in hepatic AVP trapping which is rapidly saturated due to a cold-induced depression of AVP transport and degradation. Support for this thesis was provided by finding that high AVP concentrations depressed the cold-endhancing removal phase.
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PMID:Removal of immunoreactive arginine vasopressin by the perfused rat liver. 735 52

Potassium-induced cortical spreading depression (CSD) on prostaglandin E1 (PGE1) induced fever has been investigated in a dose-responsive experimental design in both conscious and urethane-anesthetized adult male Sprague-Dawley rats. While CSD in itself had no effect on nonfebrile body temperature even under cold ambient conditions, CSD significantly suppressed small but not large fevers induced by intracerebroventricular PGE1. The increased oxygen consumption during fever was also reduced. We also explored the possible involvement of the antipyretic peptide arginine vasopressin, in the CSD-induced suppression of fever. Long term castrated rats have significantly reduced ventral septal levels of this peptide, yet CSD was effective in suppressing the initial 40 min of PGE1 fever in these animals. Thus we conclude that increased release of ventral septal arginine vasopressin is probably not involved in the action of CSD on fever.
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PMID:Effect of potassium-induced cortical spreading depression on prostaglandin-induced fever in conscious and urethane-anesthetized rats. 782 79

We determined the effect of a centrally administered V1 receptor antagonist of arginine vasopressin on the brain water content in an animal model of vasogenic brain edema. Using adult rats, a cold injury was induced in the left hemisphere of the brain by applying a frozen copper rod. 50 ng of V1 receptor antagonist was administered into the left lateral ventricle 10 minutes prior to and/or 1 hour after injury. Twenty four hours after the cold injury, the brain water and sodium contents and plasma osmolality were measured. The V1 receptor antagonist significantly suppressed the increase of the brain water and sodium contents in the cortical structure adjacent to the lesion without any changes in plasma osmolality. Our results demonstrate the effectiveness of a V1 receptor antagonist of vasopressin on vasogenic brain edema.
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PMID:Treatment of vasogenic brain edema with arginine vasopressin receptor antagonist--an experimental study. 797 30

Renal alpha 2-adrenoreceptors modulate the hydrosmotic action of arginine vasopressin (AVP) through suppression of AVP-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) accumulation. Circulating catecholamines, likely candidates for the endogenous ligand, are elevated during cold exposure (CE). These studies therefore tested the hypothesis that the diuresis observed with acute CE in rats is due in part to modulation of AVP's tubular action via alpha 2-adrenoceptor activation. Subjects were five male Brattleboro homozygous diabetes insipidus (DI) rats (358 +/- 8 g) receiving chronic AVP replacement (1 microgram.kg-1 x day-1) and seven Long-Evans (LE) normal rats (395 +/- 5 g). In a CE protocol, baseline measurements at room temperature (RT, 24 +/- 0.3 degrees C) were followed by 60-min exposure to 5 +/- 0.5 degrees C. Results were compared with those from a RT time control protocol. The selective alpha 2-antagonist yohimbine (YOH; 10 micrograms.kg-1 x min-1) or vehicle (VEH) was infused throughout the CE and RT protocols. In VEH-infused rats, CE increased urine flow by 63 +/- 12 (DI rats) and 31 +/- 4 microliters.min-1 x 100 g body wt-1 (LE rats), and mean arterial pressure by 36 +/- 1 (DI rats) and 32 +/- 2 mmHg (LE rats). The increased flow was largely a water diuresis, with changes in free water clearance averaging 45 +/- 11 (DI rats) and 28 +/- 3 microliters.min-1 x 100 g body wt-1 (LE rats). YOH treatment completely blunted the cold-induced diuresis in both strains but did not alter the CE-induced hypertension. Glomerular filtration rate was not affected by either CE or YOH infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alpha 2-adrenoceptor antagonism attenuates the diuretic response to acute cold exposure. 810 4

Centrally released arginine vasopressin (AVP) has been reported to increase the water permeability of brain capillaries under both normal and pathological conditions. It is not known, however, whether AVP regulates the permeability of brain capillaries via a V1 receptor or a V2 receptor. In the present experiments, we attempted to suppress cold-induced brain edema with V1 or V2 receptor antagonists. Adult rats were intraventricularly administered with 5 ng, 50 ng, or 500 ng of V1 receptor antagonist, or 50 ng or 500 ng of V2 receptor antagonist. Ten minutes after administration, a cold injury was induced in the left hemisphere of the brain by applying a freezing probe, which had been cooled by liquid nitrogen, to the left parietal skull for 20 seconds. Brain water and tissue sodium content were then measured 24 hours after the cold-injury. In experiment 1, the brain water content had significantly increased in both the injured and non-injured hemispheres. The administration of 50 ng of V1 receptor antagonist resulted in a significant reduction in the brain water content of the bilateral hemispheres. Administration of 50 ng of V2 receptor antagonist produced a significant reduction in the brain water content of the non-injured hemisphere only. A 500 ng administration of both antagonists did not change the brain water content of the bilateral hemispheres. In experiment 2, we divided the cold injured brain into cortical and deep structures and observed the effect of the V1 receptor antagonist. Cold-injury induced significant increases in brain water and the tissue sodium content of the bilateral cortical structures, but no changes in bilateral deep structures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of arginine vasopressin receptor antagonist on the rat cold-injured brain]. 825 20

A 65-year-old man visited our hospital with complaints of tingling sensation in the distal parts of his extremities and dysuria, which first appeared 2 months before admission. He had no abnormal findings on physical examination. Neurological examination revealed sensory impairment of glove and stocking type, mild motor weakness and muscular atrophy in the proximal parts of arms and legs, and absent tendon reflexes in knees and ankles. Fasciculation was observed on his shoulders and upper extremities, and myokymia on the abdominal wall and bilateral calves. He had hyponatremia, which was proved to be caused by SIADH. Anti-acetylcholine receptor antibody, anti-GM1 ganglioside antibody and anti-galactocerebroside antibody were detected in the serum. Chest X-ray showed mass shadows in the mediastinum, which were confirmed as malignant thymoma by needle biopsy. Orthostatic hypotension, neurogenic bladder and anhidrosis were observed by the autonomic function tests. Lesions responsible for orthostatic hypotension and SIADH were suspected in the afferent fibers from baroreceptors, since an reactive increase of plasma arginine vasopressin to orthostatic hypotension was blunted and reflex hypertension in the cold pressor test was well-preserved, while overshoot in Valsalva's maneuver was absent. It is important that afferent baroreceptor dysfunction may be associated with paraneoplastic neurological syndrome, since lesions in acute autonomic neuropathy are usually in the efferent fibers.
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PMID:[A case of paraneoplastic autonomic and sensorimotor neuropathy with dysfunction in the afferent limb of baroreflex arc]. 840 86

Tritiated arginine vasopressin ([3H]-AVP) labelled specific loci of murine renal medulla and ovine adrenal cortex in thin sections of an autoradiographic experiment. The label was fully displaced by 2 x 10(-6) M cold ligand in the case of renal, but not of adrenal sections. 10 and 100 microM AVP, however, partially displaced the radioactivity also from labelled adrenal sections. At room temperature, the half maximal blackening of the film occurred at a concentration of 26 +/- 0.9 microM. In binding experiments employing AVP and adrenocortical cell membranes, the model assuming two saturable binding sites yielded a significantly better fit than the one-site model. The equilibrium dissociation constants of ice-cold membrane preparations were 8.67 nmol/l for the high affinity site and 3.16 mumol/l for the low affinity binding site. It is concluded that the low affinity binding is governed by laws of chemical equilibrium, rather than by surface adsorption or similar "nonspecific" phenomena. When such low affinity sites are present in a tissue, higher concentrations of cold ligand ought to be used before a nondisplaceable binding is ascribed as "non-specific" or "irreversible".
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PMID:Vasopressin receptors in adrenal cortex of sheep: does autoradiography indicate an irreversible binding of the ligand? 845 Apr 94

Blood pressure stability is better during cold hemodialysis (HD). This has mainly been attributed to a more pronounced sympathetic activation during cold than during warm HD. The authors studied the effect of dialysate temperature on vasoactive peptides, noradrenaline (NA), and renin (PRA). Ten hemodynamically stable patients were dialyzed for 240 min with each of two dialysate temperatures: 38.5 degrees C (warm HD = WHD) and 34.5 degrees C (cold HD = CHD). A decrease (P < 0.05) in blood pressure occurred during WHD; however, during CHD, blood pressure was stable. There were no differences in vasoconstrictors between the two regimens. There was a decrease in NA (P < 0.05), a tendency of PRA to increase (NS owing to a large statistical spread), while arginine vasopressin was unchanged. During CHD, there was a small increase in neuropeptide Y (NPY); however, during WHD, NPY only tended to increase. However, the relative NPY levels (percent of baseline levels) after WHD and CHD did not differ. The vasodilator response was similar during both treatments. Calcitonin gene related peptide was unaltered. Motilin tended to decrease initially, but then increased (P < 0.05) to baseline levels. An increase occurred in beta-endorphin (P < 0.05) and substance P(P < 0.01). There was an initial rise (P < 0.05) in vasoactive intestinal peptide (VIP), followed by a tendency to decrease during the remainder of treatment. The authors concluded that blood pressure stability was better during CHD. However, this was not reflected by differences in plasma levels of the vasoactive peptides, nor did they find any difference in the sympathetic drive between the two regimens.
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PMID:Dialysis fluid temperature and vasoactive substances during routine hemodialysis. 855


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