ABSTRACT
SUMMARY: The expression of aquaporin-1 (AQP1) in choroid plexus and aquaporin-4 (AQP4) in astrocyte of the hippocampal formation (HF) was studied in the rat to determine the role of AQP1 and AQP4 in the pathophysiology of systemic hyponatremia (SH). SH was induced by coadministration of dextrose solution intraperitoneally and through subcutaneous implantation of an osmotic minipump containing 8-deamino-arginin vasopressin (50ng/µl/h) for 24 and 48 h. Twenty- four and 48 h after the drug administration, there were significant reductions in Na+ concentration (111 ± 5 and 104 ± 2 mmol) and serum osmolarity (240 ± 13 and 221 ± 14 mOsm/L) as compared with control values (140 ± 4.7 mmol and 296 ± 5.2 mOsm/L), (p<0.01). The expression of AQP1 in the choroid plexus was increased three to five times from 24 h to 48 h after SH (329.86 ± 10.2 % and 531.5 ± 4.4 %, n=4, p<0.01). In contrast, AQP4 expression was significantly decreased up to 48 h after SH (36 ± 9 %, n=4, p<0.01). Quantitative immunoblotting revealed significant decreases of neuronal proteins in the HF after 24 to 48 h of SH. Therefore, we suggest that altered expression of AQP1 and AQP4 plays important role in the pathogenesis of systemic hyponatremia.
RESUMEN: En este análisis se estudió la expresión de acuaporina-1 (AQP1) en plexo coroideo y acuaporina-4 (AQP4) en astrocitos de la formación hipocampal (FH) en ratas para determinar el papel de AQP1 y AQP4 en la fisiopatología de la hiponatremia sistémica (HS). La HS fue inducida mediante la coadministración de solución de dextrosa por vía intraperitoneal y mediante la implantación subcutánea de una minibomba osmótica que contenía vasopresina 8-desaminoarginina (50 ng /µ l / h) durante 24 y 48 h. Veinticuatro y 48 h después de la administración del fármaco, hubo reducciones significativas en la concentración de Na + (111 ± 5 y 104 ± 2 mmol) y la osmolaridad sérica (240 ± 13 y 221 ± 14 mOsm /µL) en comparación con los valores de control (140 ± 4,7 mmol y 296 ± 5,2 mOsm / L), (p <0,01). La expresión de AQP1 en el plexo coroideo se incrementó de tres a cinco veces de 24 a 48 h después de HS (329,86 ± 10,2 % y 531,5 ± 4,4 %, n = 4, p <0,01). Por el contrario, la expresión de AQP4 se redujo significativamente hasta 48 h después de HS (36 ± 9 %, n = 4, p <0,01). La inmunotransferencia cuantitativa reveló disminuciones significativas de proteínas neuronales en el FH después de 24 a 48 h de SH. Por lo tanto, sugerimos que la expresión alterada de AQP1 y AQP4 juega un papel importante en la patogénesis de la hiponatremia sistémica.
Subject(s)
Animals , Rats , Brain/metabolism , Aquaporin 1/metabolism , Aquaporin 4/metabolism , Hyponatremia/metabolism , Immunoblotting , Rats, Sprague-Dawley , Electrophoresis, Polyacrylamide GelABSTRACT
El desarrollo de la hiponatremia en la comunidad es un aspecto poco estudiado, y su frecuencia y los factoresque la condicionan son poco conocidos. Objetivos: Estudiar los factores clínicos y de laboratorio asociados a la hiponatremia de pacientes incidentes en el servicio de emergencia de un hospital general. Material y métodos: Estudio de casos y controles. Los casos fueron pacientes con Na+ sérico5 mg/dl. Se contrastaron las variables edad, sexo, sistemas comprometidos, gravedad del paciente y valor de loselectrolitos; gases arteriales; urea y creatinina. El tamaño de muestra fue de 20 casos y 40 controles (confianza 95%, potencia 80% y OR 4)...
The prevalence and associated factors for developing hyponatremia in the community have not been adequately studied. Objectives: To study the clinical and laboratory factors associated with hyponatremia in patients attending the emergency room of a general hospital. Methods: A case-control was carried out, cases were patients with serum sodium values below 135 mEq/l at the time of admission to the emergency room of Hospital Cayetano Heredia and controls were patients admitted at the same time as cases with serum sodium values from 135 y 145 mEq/l. Patients with serum creatinine values >5 mg/dl were excluded...
Subject(s)
Humans , Alkalosis/metabolism , Electrolytes/metabolism , Hyponatremia , Hyponatremia/metabolism , Sodium/metabolism , Case-Control StudiesABSTRACT
ABSTRACT OBJECTIVES: To study the effect of two intravenous maintenance fluids on plasma sodium (Na), and acid-base balance in pediatric intensive care patients during the first 24 h of hospitalization. METHODS: A prospective randomized controlled study was performed, which allocated 233 patients to groups: (A) NaCl 0.9% or (B) NaCl 0.45%. Patients were aged 1 day to 18 years, had normal electrolyte concentrations, and suffered an acute insult (medical/surgical). Main outcome measured: change in plasma sodium. Parametric tests: t-tests, ANOVA, X 2 statistical significance level was set at a = 0.05. RESULTS: Group A (n = 130): serum Na increased by 2.91 (±3.9) mmol/L at 24 h (p < 0.01); 2% patients had Na higher than 150 mmol/L. Mean urinary Na: 106.6 (±56.8) mmol/L. No change in pH at 0 and 24 h. Group B (n = 103): serum Na did not display statistically significant changes. Fifteen percent of the patients had Na < 135 mmol/L at 24 h. The two fluids had different effects on respiratory and post-operative situations. CONCLUSIONS: The use of saline 0.9% was associated with a lower incidence of electrolyte disturbances.
RESUMO OBJETIVO: Estudar o efeito de dois fluidos de manutenção intravenosos sobre o sódio (Na) plasmático e o equilíbrio ácido-base em pacientes de terapia intensiva pediátrica durante as primeiras 24 horas de internação. MÉTODOS: Foi feito um estudo controlado randomizado prospectivo. Alocamos aleatoriamente 233 pacientes para os grupos: (A) NaCl a 0,9% e (B) NaCl a 0,45%. Os pacientes com um dia a 18 anos apresentavam concentrações normais de eletrólitos e sofriam de insulto agudo (médico/cirúrgico). Principal resultado: variação no sódio plasmático. Testes paramétricos: teste t, Anova, qui-quadrado. O nível de relevância estatística foi estabelecido em a = 0,05. RESULTADOS: Grupo A (n = 130): o Na sérico aumentou 2,91 (± 3,9) mmol L-1 em 24 h (p < 0,01); 2% dos pacientes apresentaram Na acima de 150 mmol L-1. Concentração média de Na na urina: 106,6 (± 56,8) mmol L-1. Sem alteração no pH em 0 e 24 horas. Grupo B (n = 103): o Na sérico não apresentou alterações estatisticamente significativas; 15% dos pacientes apresentaram Na < 135 mmol L-1 em 24 h. Os dois fluidos tiveram efeitos diferentes sobre as situações respiratória e pós-operatória. CONCLUSÃO: O uso de solução fisiológica a 0,9% foi associado à menor incidência de distúrbios eletrolíticos.
Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Male , Acid-Base Equilibrium/drug effects , Fluid Therapy/methods , Sodium Chloride/pharmacology , Sodium/metabolism , Fluid Therapy/adverse effects , Hyponatremia/chemically induced , Hyponatremia/drug therapy , Hyponatremia/metabolism , Infusions, Intravenous , Intensive Care Units, Pediatric , Prospective Studies , Sodium Chloride/metabolism , Sodium/bloodABSTRACT
Most sodium disturbances in patients with CNS lesions result from disturbed water regulation. Possible systemic and iatrogenic causes must be evaluated prior to treatment. Insufficient secretion of ADH leads to hypernatremia if fluid intake is inadequate and can be treated with either fluid or hormone replacement. Care must be exercised in patients with acute diabetes insipidus because of the potentially variable and transient nature of the disturbance. Hyponatremia usually results from inappropriate secretion of ADH and should be managed aggressively in symptomatic patients with loop diuretics and hypertonic saline. However, very rapid correction or overcorrection should be avoided. Patients with SAH and hyponatremia should not be fluid restricted because of the risk of exacerbating vasospasm but treated with large volumes of isotonic or mildly hypertonic saline.
Subject(s)
Diabetes Insipidus/metabolism , Humans , Hypernatremia/metabolism , Hyponatremia/metabolism , Intensive Care Units , Nervous System Diseases/blood , Sodium/blood , Water-Electrolyte Imbalance/complicationsABSTRACT
Se presenta escolar de 9 años, sexo masculino con una hemorragia subaracnoida secundario a malformación vascular dorsolumbar: Evoluciona con hipovolemia severa, natriuveris y tendencia a la hiponatremia lo que hace plantear Síndrome Cerebral Perdedor de Sal (SCPS). Se manejó con aporte extra de sodio y fármaco con propiedades mineralocorticoides (Fluorhidrocortisona) con lo cual se observa mejoría. Alrededor de 1988 se plantea por primera vez este síndrome, presentándose entre el 9 y el 33 por ciento de los pacientes con hemorragia subaracnoídea. Dado lo difícil que resulta precisar la causa de la hiponetremia en estos pacientes se expone las características clínicas, fisiopatológicas y manejode esta afección