The Hypocalcemic Effect of Ethyl Alcohol in Rats and Dogs1

Abstract

Oral administration of ethyl alcohol in doses of 2-8 g/kg bw produced a rapid and sustained hypocalcemia in rats and dogs. The rapid onset (within 30 min) and the long duration (at least 5 hr) of hypocalcemia in rats after alcohol were characteristics similar to those we had observed previously with urethane. In control experiments, addition of alcohol to rat serum did not interfere with the analytical method for measurement of calcium. Furthermore, under the experimental conditions studied no changes in blood pH or total serum proteins occurred. The hypocalcemic effect of alcohol could not be explained by increased loss of urinary calcium, because the effect was retained after acute nephrectomy and because direct measurement of urine calcium revealed that ethanol decreased rather than increased total urinary calcium during a 3–hr time interval after treatment. The hypocalcemic action of alcohol differed from that of thyrocalcitonin; (a) the hypocalcemia caused by alcohol was not associated with hypophosphatemia, and (b) the maximum hypocalcemic effect of alcohol in rats was only 10–15% in contrast to the 30–40% fall in serum calcium which can be produced by thyrocalcitonin. The hypocalcemic effect of alcohol was evident after acute removal of the thyroid and parathyroid glands. Therefore, the effect of alcohol was not mediated by increased secretion of thyrocalcitonin or by suppression of secretion of parathyroid hormone. Experiments using 45Ca showed that alcohol caused a movement of calcium out of blood, presumably into some tissue, most likely bone. The coincidence between the occurrence of hypocalcemia and of anesthesia after large doses of alcohol suggests that the neural effects of alcohol and its ability to lower serum calcium may be interrelated. (Endocrinology91: 586, 1972)