Osmotic regulation of estrogen receptor-beta in rat vasopressin and oxytocin neurons.
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The vasopressin (VP) magnocellular neurosecretory cells (MNCs) in the supraoptic and paraventricular (PVN) nuclei are regulated by estrogen and exhibit robust expression of estrogen receptor (ER)-beta. In contrast, only approximately 7.5% of oxytocin (OT) MNCs express ER-beta. We examined the osmotic regulation of ER-beta mRNA expression in MNCs using quantitative in situ hybridization histochemistry. Hyper-osmolality induced via 2% hypertonic saline ingestion significantly decreased, whereas sustained hypo-osmolality induced via d-d-arginine VP and liquid diet increased ER-beta mRNA expression in MNCs (p < 0.05). Thus, the expression of ER-beta mRNA correlated inversely with changes in plasma osmolality. Because hyper-osmolality is a potent stimulus for VP and OT release, this suggests an inhibitory role for ER-beta in MNCs. Immunocytochemistry demonstrated that the decrease in ER-beta mRNA was translated into depletion of receptor protein content in hyper-osmotic animals. Numerous MNCs were positive for ER-beta in control animals, but they were virtually devoid of ER-beta-immunoreactivity (IR) in hyper-osmotic animals. The osmotically induced decrease in ER-beta expression was selective for MNCs because ER-beta-IR remained unaltered in PVN parvocellular neurons. Plasma estradiol and testosterone were not correlated with ER-beta mRNA expression after osmotic manipulation, suggesting that ER-beta expression was not driven by ligand availability. Expression of FOS-IR in MNCs with attenuated ER-beta-IR, and the absence of FOS-IR in parvocellular neurons that retain ER-beta-IR suggest a role for neuronal activation in the regulation of ER-beta expression in MNCs. Thus, osmotic modulation of ER-beta expression in MNCs may augment or attenuate an inhibitory effect of gonadal steroids on VP release. (+info)
BORIC ACID POISONING: REPORT OF 11 CASES.
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Boric acid poisoning in 11 infants, occurring in the newborn nursery as a result of the accidental and inadvertent use of 2.5% boric acid in the preparation of the formulae, is reported. Five of the infants died. All except two exhibited the classical symptomatology of acute boric acid poisoning, namely, diarrhea, vomiting, erythema, exfoliation, desquamation of the skin, and marked central nervous system irritation. Early manifestations of poisoning were nonspecific, and one patient died before skin manifestations were noted. Peritoneal dialysis, instituted in nine cases, was found to be the most effective method of treatment. It is recommended that boric acid, which is of doubtful therapeutic value, should be completely removed from hospitals, dispensaries and pharmacopoeias. (+info)
Neonatal weight loss in breast and formula fed infants.
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OBJECTIVE: To define the range of neonatal weight loss in a population relative to feeding method. DESIGN: Prospective observational cohort study. SETTING: Maternity service providing geographically defined, community based newborn follow up. PARTICIPANTS: 971 consecutive term newborns of birth weight > or = 2500 g during the first 2-3 weeks of life; 34 excluded (inadequate data). 937 included: 45% breast fed, 42% formula fed, 13% breast and formula fed. OUTCOME MEASURES: Maximum weight loss and timing, age on regaining birth weight. RESULTS: Median weight loss: formula fed 3.5%, breast fed 6.6%. Upper centiles for maximum weight loss differ considerably (95th centiles: breast fed = 11.8%, formula fed = 8.4%; 97.5th centiles: breast fed = 12.8%, formula fed = 9.5%). Median time of maximum weight loss: 2.7 days for breast fed and formula fed. Recovery of birth weight: breast fed median 8.3 days, 95th centile 18.7 days, 97.5th centile 21.0 days; formula fed median 6.5 days, 95th centile 14.5 days, 97.5th centile 16.7 days. The time taken to regain birth weight correlates with both the degree and timing of initial weight loss for all groups. CONCLUSIONS: Early neonatal weight loss is defined allowing identification of infants who merit closer assessment and support. (+info)
New insights into the pathophysiology of the dysnatremias: a quantitative analysis.
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Recent theoretical considerations have played an important role in advancing our understanding of the physiological mechanisms responsible for perturbing the plasma water sodium concentration ([Na(+)](pw)) in health and disease. Central to these considerations is the original empirical relationship between the [Na(+)](pw) and total exchangeable sodium (Na(e)), total exchangeable potassium (K(e)), and total body water (TBW) initially discovered by Edelman and colleagues (Edelman IS, Leibman J, O'Meara MP, and Birkenfeld LW. J Clin Invest 37: 1236-1256, 1958). The non-zero values of the slope and y-intercept in the Edelman equation are a consequence of the effects of the osmotic coefficient of Na(+) salts at physiological concentrations and Gibbs-Donnan and osmotic equilibrium. Moreover, in addition to Na(e), K(e), and TBW, the physiological components of the y-intercept in this equation play a role in modulating the [Na(+)](pw) and in the generation of the dysnatremias. In this review, the pathophysiological mechanisms underlying the generation and treatment of the dysnatremias are analyzed theoretically and quantitatively. Importantly, the non-zero values of both the slope and y-intercept in the Edelman equation result in several theoretical predictions that can be tested experimentally and have been mathematically incorporated into recently derived equations used to analyze both the generation and the optimal treatment of the dysnatremias. In addition, we review current concepts regarding 1) the role of Gibbs-Donnan and osmotic equilibrium in the determination of the [Na(+)](pw); 2) the modulating effect of osmotically inactive exchangeable Na(+) and K(+) on the [Na(+)](pw); 3) the effect of glucose on the [Na(+)](pw) as reflected by changes in Na(e), K(e), and TBW as well as changes in several components of the y-intercept resulting from the hyperglycemia; and 4) the complex role of K(+) in modulating the [Na(+)](pw). (+info)
Collecting duct-specific knockout of endothelin-1 causes hypertension and sodium retention.
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In vitro studies suggest that collecting duct-derived (CD-derived) endothelin-1 (ET-1) can regulate renal Na reabsorption; however, the physiologic role of CD-derived ET-1 is unknown. Consequently, the physiologic effect of selective disruption of the ET-1 gene in the CD of mice was determined. Mice heterozygous for aquaporin2 promoter Cre recombinase and homozygous for loxP-flanked exon 2 of the ET-1 gene (called CD-specific KO of ET-1 [CD ET-1 KO] mice) were generated. These animals had no CD ET-1 mRNA and had reduced urinary ET-1 excretion. CD ET-1 KO mice on a normal Na diet were hypertensive, while body weight, Na excretion, urinary aldosterone excretion, and plasma renin activity were unchanged. CD ET-1 KO mice on a high-Na diet had worsened hypertension, reduced urinary Na excretion, and excessive weight gain, but showed no differences between aldosterone excretion and plasma renin activity. Amiloride or furosemide reduced BP in CD ET-1 KO mice on a normal or high-Na diet and prevented excessive Na retention in salt-loaded CD ET-1 KO mice. These studies indicate that CD-derived ET-1 is an important physiologic regulator of renal Na excretion and systemic BP. (+info)
Factors during donor care that may affect liver transplantation outcome.
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Publications are reviewed that identify factors during donor care and characteristics of the donor liver that may be associated with outcome following liver transplantation. The procurement coordinator has the opportunity to influence cold ischemia time, blood pressure, the serum sodium concentration and, perhaps, liver glycogen reserves. These variables may significantly affect postimplantation graft performance and graft or recipient survival. Summaries of those publications comprising this database are presented, and several limitations in their interpretation are discussed. (+info)
A non-fatal case of sodium toxicity.
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A non-fatal case of sodium toxicity in a six-year-old boy is presented. Hypernatremia is the clinical term for an excessive concentration of sodium relative to water in the body. The diagnosis of hypernatremia was made at serum sodium (Na(+)) concentrations exceeding 150 mEq/L, and few people have been reported to survive concentrations greater than 160 mEq/L. This case involves a six-year-old boy who was taken to the hospital following a seizure attack, and lab analyses revealed serum sodium (Na(+)) levels of 234 mEq/L and serum chloride (Cl(-)) levels of 205 mEq/L. Clinical tests ruled out diabetes insipidus, dehydration, renal pathology, and other primary causes of hypernatremia. The child's purported history of pica, and the lab results indicating corresponding increases in levels of serum sodium (Na(+)) and serum (Cl(-)), led to a diagnosis of acute sodium toxicity by ingestion of sodium chloride. A search of the boy's house led to the discovery of rock salt in the cabinet and a container of table salt. Extrapolating from the serum sodium (Na(+)) level, it was estimated that the child had ingested approximately four tablespoons of rock salt, leading to the acute toxicity. A literature search revealed that the serum sodium (Na(+)) concentration in the present report was the highest documented level of sodium in a living person. (+info)
The case of the floating gel.
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In patients with chronic renal failure, blood samples for laboratory analysis are often taken via dialysis catheters. This report describes a case of gross spurious hypernatraemia in a blood sample collected from a patient undergoing haemodialysis. After centrifugation of the blood sample in question, the separator gel formed the topmost layer, with the serum in the middle and the clot at the bottom. Subsequent analysis of the serum showed severe hypernatraemia (serum sodium, 744 mmol/litre). It was established that the blood sample had been taken from the patient's dialysis catheter into which 3 ml of Citra-Lock (46.7% trisodium citrate) had been instilled previously as a "catheter locking" solution. The hypernatraemia seen in this case was recognised immediately as an artefact, but it was found that even minimal contamination of blood samples with Citra-Lock may significantly affect sodium concentrations. This contamination may be missed, with potentially adverse consequences for patient management. (+info)