Biomedical subjects
Publications and source records attributed to L F de la Cruz.
We studied whether or not mast cells are endowed with specific sodium channels, by using tritiated saxitoxin which binds to site 1 of sodium channels on excitable tissues. Our results suggest that rat pleural and peritoneal mast cells lack specific sodium channels.
Exposure of rat mast cells to isotonic sucrose (employed as a sodium free medium) increased several-fold the sensitivity to calcium, which itself became a stimulus for exocytosis. Concentrations of the cation as low as 25 microM permitted maximal histamine release. Preincubation of cells in sucrose to allow sodium efflux before adding the ionophore A23187 led to a slower release of histamine. We postulate that sodium efflux can generate a membrane potential that causes the increased sensitivity to calcium and the delay in response after preincubation. The response to A23187 is somewhat unspecific since the ionophore can release histamine from internal calcium reservoirs. Saxitoxin or veratridine did not affect cell responses, so that sodium activity is not mediated through defined sodium channels.
Rat lung mast cells were stimulated with drugs with distinct mechanisms of action, namely concanavalin A, compound 48/80 ionophore A23187, in the presence of the beta adrenergic agonist (-)isoproterenol. Cells show a high response when they are stimulated with FNa-calcium. Isoproterenol does not inhibit histamine release induced by any stimuli, but enhances the response to concanavalin A and compound 48/80. Results point to the lack of beta activity on rat lung mast cells.
Enzymatically isolated dog lung and gut mast cells were stimulated with compound 48/80, ionophore A23187, concanavalin A and FNa-Ca. Cell response elicited by A23187, concanavalin A or 48/80 is almost completely inhibited by isoproterenol. Concanavalin A induced histamine release on gut mast cells is high, indicating an elevated degree of sensitization of these cells. Results point to the existence of beta adrenergic inhibitory activity on dog lung and gut mast cells.
The effects produced in offspring by corticosterone treatment to breeder quail were investigated. The breeders received corticosterone orally every day during 7 days. The total dose administered was 3.15 mg/quail/7 days. The quail from treated breeders have a decreased rate of body growth during the experimental period. The studied metabolic and nutritives parameters were smaller than the control group, however, the relative indices were similar. The breeders treated with corticosterone produce quail smaller than controls, but the pattern during the growth period is similar, there it can be observed by the same relative indices.
Serum concentration evolution of thyroxine and triiodothyronine, and thyrotropin (TSH), have been studied in rats while they were given 6-propylthiouracil (PTU) as antithyroid drug, and during the recovery period after suppression of treatment. In the same way thyroid hypertrophy and plasmatic levels of thyrotropin were correlated. Animals received orally a daily dose of 1 mg/100 g body weight during thirty-five days and had a two week recovery period. Thyroid hormone concentrations in plasma were determined by immunoenzymatic assay ELISA with peroxidase as labelled enzyme. From the results obtained, it can be stated that chronic administration of PTU implies a continuous decrease in thyroid hormone concentrations in plasma, reaching nearly zero values, while after treatment, levels recover their normal values in a week's time. A parallelism exists between thyroid hypertrophy and pituitary TSH hypersecretion, due to a decrease in thyroid hormone levels.
The effects of glucocorticoids on nitrogen metabolism have been studied in three different groups of quail: a) control animals; b) quail treated with cortisol; c) quail treated with corticosterone. All the experiments were carried out in adult male and non-laying female animals. During the 7 day period that the experiments lasted, hormones were administered daily by via oral at 4 mg/100 g body weight/7 day doses. While body weight, food intake, nitrogen balance and liver weight, in the treated animals stayed under the values of the control group, in both males and females, their uric acid excretion and hepatic glycogen were always higher. Values, in general, were similar for both males and females.