Abstract

Acute ethanol loading in the rat induces hypocalcemia and hypermagnesemia. In addition, hypocalcemia is not corrected by exogenous PTH. In the rat the mechanism of these changes was investigated by measuring plasma immunoreactive parathyroid hormone (PTH). PTH was also measured in culture medium in which parathyroid glands were incubated. The addition of ethanol to test tubes did not interfere with PTH measurement. Absolute ethyl alcohol diluted to 50% with distilled water was administered via an intragastric tube. It failed to induce an increase in plasma immunoreactive PTH level. Similarly, it prevented an increase in plasma PTH after disodium EDTA injection. Thus in the presence of ethyl alcohol plasma PTH failed to increase in spite of a significant decrease of plasma calcium. In vitro studies showed that the decrease of calcium concentration of the medium from 1.50 to 0.75 mmol/l was associated with a 3 to 5 times increase in PTH secretion rate. This increase was suppressed when ethanol was added to the culture medium. In conclusion, ethanol loading via gastric tubing induced: 1) decrease in plasma calcium; 2) suppression of immunoreactive PTH secretion in the presence of hypocalcemia. It is postulated that the acute hypocalcemic effect of ethanol loading is mediated by a dual effect at the level of the bone and the parathyroid gland.

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