Sucrose electrolyte solution for oral rehydration in diarrhea.
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Biomedical subjects
Publications and source records attributed to J E Rohde.
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With attack rates exceeding two episodes per year in the young diarrhoea with attendant dehydration is by far the major single killer in the developing world. An invariable accompaniment of the more insidious and chronic protein-energy malnutrition (PEM), diarrhoea is itself an acute form of malnutrition: fluid-electrolyte malnutrition (FEM). Scientific attention to FEM has focused heavily on mechanisms of pathogenesis and disordered physiology, often to the neglect of preventive and effective control measures. A notable exception was the huge step from the short-circuit chamber to the cholera ward which carried the science of coupled transport to the field. Glucose-electrolyte solutions provide effective prevention and treatment of dehydration and, where combined with early proper feeding, an interruption of the FEM-PEM cycle. Wider use of this simple technology awaits greater understanding and interact-on with the social systems that determine the ecology of diarrhoeal disease.
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Increased permeability of the intestinal mucosa to small molecules and ions has previously been proposed as a mechanism causing the profuse diarrhoea characteristic of Asiatic cholera. A technique for measuring absorption rates of (14)C-urea and (3)H-arabinose has been employed to study jejunal permeability during experimental canine and naturally acquired human cholera. The ratio of the absorption rates of these two solutes of different size is an expression of intestinal membrane selectivity and permits calculation of an equivalent pore radius. No change of membrane selectivity was observed in canine loops after challenge with cholera toxin. During naturally acquired human cholera, jejunal pore size was not significantly different from that measured during convalescence. This method was demonstrated to be sensitive to changes induced by amphotericin B, an antibiotic known to alter membrane permeability and selectivity. These data are inconsistent with the hypothesis of increased intestinal permeability during cholera.
This study demonstrated that endogenous aldosterone, as determined by its transient competitive block by spironolactone, caused significant sodium and chloride retention during naturally acquired cholera. This beneficial effect of the hormone is accompanied, however, by a deleterious depletion of potassium. In addition, it was found that stool rate significantly altered the sodium and potassium concentrations in cholera stool despite minimal or absent aldosterone activity.