In-vitro basophil degranulation in drug-suspected acute renal failure.
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Biomedical subjects
Publications and source records attributed to L Hernando.
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The effect of papaverine at the time of starting a post-ischemic acute renal failure in rats has been studied. Papaverine administration increases diuresis and reduces serum urea and creatinine levels. The primary role of hemodynamic disorders as responsible for the diminished glomerular filtration rate is supported by the reduced severity of acute renal failure when this vasodilator agent is administered.
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The effect of nearly total renal ischemia during a two hour period on glomerular filtration and urine composition was studied in relation to tubular permeability and tubular obstruction, two mechanisms that could explain renal insuficiency after iscehmia. Studies on creatinine clearance, micropuncture and microinjection of 14C-inulin into the proximal tubules by means of a hydraulic system were performed before and after the period of ischemia. Thirty minutes after the withdrawal of arterial obstruction, the animals exhibited a maintained diuresis, 50 per cent reduction in glomerular filtration in the superficial nephrons and in the total kidney, a reduction in the proximal fractional absorption of water, and also an increase in the urinary elimination of sodium. The glomerular filtrate of cortical nephorns obtained by micropuncture in anterior areas of the proximal tubules did not differ significantly from the one obtained by micropuncture in more distal areas. The inulin injected into the proximal tubules of a kidney was entirely eliminated by it.
Furosemide and acetazolamide effects on tubular function in rat kidney have been studied by micropuncture. Furosemide produced a marked rise in fractional proximal fluid reabsorption when urine loss was not replaced, and sodium excretion rose significantly indicating a distal effect. If urinary losses were replaced proximal fractional reabsorption was depressed and fractional sodium excretion increased more than 60%. After replacing urinary losses, acetazolamide had a greater depressive effect on proximal tubular fluid reabsorption than furosemide but sodium excretion values were about 1/3 of those obtained with furosemide. Superimposition of one drug during the action of the other resulted in potentiation of proximal inhibition, suggesting a different mechanism of action. The changes observed in potassium excretion are of great interest. Separately, furosemide or acetazolamide produced kaliuresis. When furosemide was administered during acetazolamide diuresis, however, potassium excretion was reduced despite the sharp rise in sodium excretion.
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24% of a healthy control population had antibody to hepatitis-B surface antigen (HBsAb) detectable by passive haemagglutination. The frequency was higher in other population groups in proportion to the intensity of contract with individuals or material positive for HBsAg. Data obtained during an outbreak of type-B hepatitis indicate that immunity to the disease is directly dependent on the titre of circulating HBsAb. A close relationship was found between the presence of HBsAb and liver dysfunction in carriers of HBsAg. This supports the hypothesis that immune response to the antigen may be necessary for the development of liver damage in type-B hepatitis. Nevertheless, since a good antibody response to HBsAg was found in uraemic patients, in whom hepatitis had a clinical course quite different from the population at large, it is thought that immune mechanisms other than the humoral response may account for the pathogenesis of the disease.
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