Contraction alkalosis in the awake rat: study of its generation and 24-hour follow-up.
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Biomedical subjects
Publications and source records attributed to M Paillard.
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The intensity of penetrance of the vestigial gene in the progeny obtained by crossing a wild type and a vestigial strain characterizes the wild type.
A pure contraction alkalosis with no urinary loss of bicarbonate was evidenced in awaken rat, after a Furosemide IV injection. We observed: 1) an early and important respiratory compensation possibly owing to a simultaneous contraction of CSF volume, thus increasing bicarbonate concentration. 2) a net shift of HCO3- towards intracellular compartment, in proportion to the magnitude of the contraction rather than to bicarbonate gradient across the membrane.
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1. Conflicting values of intracellular pH (pH(i)) were obtained by Caldwell in crab muscle and by Carter et al. in rat muscle. To investigate this discrepancy, double and single barrelled pH sensitive micro-electrodes as described by Carter et al. were used both in rat muscle (in vivo and in vitro) and in large single fibres of crab (in vitro).2. The pH(i) values obtained in the superficial layers of muscle cells in rat and pH(i) values obtained in the superficial area of large single fibres in crab seemed in agreement with the Donnan equilibrium. Furthermore, when the membrane potential (E(m)) value of extracellular pH (pH(e)) value was changed, each new pH(i) value was obtained instantly.3. The pH(i) values obtained in deep layers of muscle cells in rat (pH(i) 6.68) and in a deep area of large single fibres in crab (pH(i) 6.96) did not agree with Donnan equilibrium; these pH(i) values were little influenced by modifications in E(m) or pH(e) values.4. These findings could be easily explained if the length of the sensitive portion of the pH micro-electrode exceeds the diameter of rat muscle cells and is smaller than the diameter of crab large fibres. The pH(i) values obtained superficially in the two preparations and which seem in agreement with the Donnan equilibrium are artificially low because the E(m) values recorded by the pH micro-electrodes are partly shunted.
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OBJECTIVE: Despite many studies, the impact of chronic insomnia on daytime functioning is not well understood. The aim of our study was to detect this impact by evaluating quality of life (QoL) using a validated instrument, the 36-item Short Form Health Survey of the Medical Outcomes Study (SF-36), in three matched groups of severe insomniacs, mild insomniacs, and good sleepers selected from the general population. METHODS: Three matched groups of 240 severe insomniacs, 422 mild insomniacs, and 391 good sleepers were recruited from the general French population after eliminating those with DSM-IV criteria for anxiety or depression. All subjects were asked to complete the SF-36. Scores for each QoL dimension were calculated and compared statistically among the three groups. RESULTS: Severe insomniacs had lower QoL scores in eight dimensions of the SF-36 than mild insomniacs and good sleepers. Mild insomniacs had lower scores in the same eight dimensions when compared with good sleepers. No dimension was significantly more altered than the other. CONCLUSIONS: The mental health status and role of emotional QoL dimensions were worse in severe and mild insomniacs than in good sleepers. This result held even though we screened for psychiatric diseases, which shows a clear interrelation between insomnia and emotional state. General health status was also worse in severe and mild insomniacs than in good sleepers. However, we could conclude only that insomnia was related to a worse health status and not whether it was a cause or consequence of this worse health status. Finally, the degradation of QoL scores was correlated with the severity of insomnia.
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The availability of accurate and inexpensive methods for measuring serum calcium levels has resulted in a rapid increase in the number of diagnoses of primary hyperparathyroidism, notably in its asymptomatic hypercalcemic forms. In addition, the development of a radioimmunoassay of the parathyroid hormone and, more recently, measurements of nephrogenous cyclic AMP during fasting and after calcium loading have led to the recognition of clinical variants of the disease, such as intermittent or borderline hypercalcemia and pure hypercalciuria with normal calcemia. The degree of hypercalcemia in stable primary hyperparathyroidism depends on renal tubular reabsorption of calcium rather than on bone resorption. The poor correlation observed between calcium tubular reabsorption rate and magnitude of parathyroid hormone hypersecretion suggests that as yet undetermined factors interfere with the effects of parathyroid hormone on renal tubules and probably account for the fluctuations in calcemia reported during serial determinations in patients. The sigmoid relationship between parathyroid hormone release and extracellular calcium concentrations has been analyzed from recent in vitro studies with dispersed parathyroid cells. In primary hyperplasia of the parathyroid glands hypersecretion of parathyroid hormone seems to depend principally upon the increase in tissue mass with normal sensitivity to calcium at cellular levels, whereas in adenoma the primary abnormality responsible for hypersecretion of parathyroid hormone would be an alteration in cell sensitivity to calcium, as indicated by an elevated "set point". Finally, while complicated primary hyperthyroidism requires surgery, our limited knowledge of the natural history of asymptomatic forms makes it impossible to decide which of these patients will ultimately need to be operated upon.