The effects of lead poisoning on calcium transport by brain in 30-day-old albino rabbits.
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Biomedical subjects
Publications and source records attributed to S L Cookson.
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The interaction of morphine sulphate and phenytoin was studied with respect to morphine-induced catalepsy in the rat using a previously described method for measuring degree of immobility. As expected, catalepsy developed several minutes after intravenous morphine and lasted for more than ninety minutes. Intravenous phenytoin, 35 mg/kg, given fifteen min prior to or following the administration of morphine, 1 mg/kg, significantly prevented, or reversed, morphine-induced catalepsy. Control experiments revealed that the antagonistic effect was due solely to the morphine-phenytoin interaction. A similar effect was found with naloxone, 0.2 mg/kg. The data are discussed in terms of possible sites of interaction, including synaptosomal calcium metabolism.
An assay for determining the DNA content of mononuclear phagocytes is described. The assay is efficient and very sensitive, measuring as little as 1 microgram of DNA. Content of DNA is a linear function of the number of mononuclear phagocytes in the sample. One million murine macrophages contain 10.1 +/- 0.36 microgram of DNA. Consequently, samples of as few as 100,000 macrophages can be accurately quantified to be related to other biochemical analyses.
Since abnormalities in the renal handling of sodium and water in both the proximal and distal tubule have been described in primary hypothyroidism, this study was undertaken to examine renal tubular hydrogen secretion in this disorder. Metabolic acidosis was induced in hypothyroid rats (H) and their age matched controls (C) by the administration of an oral ammonium chloride load of 0.15 g/24 h/kg for three days. On day 3 animals were prepared for clearance and acid-base studies, receiving an infusion of Ringer's solution of 0.6 ml/hr/100 g during surgery and the experimental procedure. A 26% decrease in GFR (P less than 0.005) and a doubling in fractional excretion of sodium (P less than 0.02) were observed in H rats. The lowest blood pH and average bicarbonate concentration and the excretion of chloride were similar in the two groups, indicating that the acid load was reabsorbed and led to similar degrees of systemic acidification. Urine flow also was comparable in the two groups. Minimal urine pH after NH4Cl was 6.21 +/- 0.06 in H and 5.68 +/- 0.09 in C (P less than 0.001). Ammonium excretion was 28% (P less than 0.05) lower in H than in C. The defect in urine acidification in H was only partially corrected after 5 days on a low sodium diet and DOCA administration for 2 days. Fractional bicarbonate excretion at normal blood pH and bicarbonate concentration was not different in the two groups. These data indicate that hypothyroid rats have a mild defect in urine acidification and that it is localized predominantly in the distal tubule.
Abnormalties in renal concentrating ability and free water reabsorption, and a diminished sodium excretion, glomerular filtration rate, and effective renal plasma flow were observed in adolescent rats which ingested a lipotrope deficient diet for 10 months.