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Plasma Catecholamines in Acute Magnesium Deficiency in Weanling Rats^1,2,

Division of Disorders of Carbohydrate Metabolism, The Human Genetics Branch, The National Institute of Child Health and Human Development, The National Institutes of Health, Bethesda, MD 20892 ^* Upjohn Diagnostics, Kalamazoo, MI 49001

A controlled study was conducted to quantitate plasma catecholamines in magnesium-deficient weanling rats experiencing the seizure-shock episode. Eighty-four male Sprague-Dawley rats each weighing 35.6 ± 0.3 g (mean ± SEM) were fed purified diets to which was added 150 mg magnesium/100 g (Mg-150) or no magnesium (Mg-0). Studies were conducted between d 5 and 8. Plasma and bone magnesium and calcium were measured by atomic absorption spectrophotometry, and plasma catecholamines by radioenzymatic assay using ³H. Compared with Mg-150 rats, the Mg-0 rats showed reduced weight gain (P < 0.001); reduced plasma magnesium (P < 0.001) and reduced bone magnesium (P < 0.001) with no corresponding changes in calcium concentration; and a 25% mortality by d 8. Pair-feeding and 80-dB noise provoked no changes in plasma catecholamines in Mg-150 rats, but both strychnine-induced seizures in Mg-150 rats and seizures induced by 80-dB noise in Mg-0 rats were accompanied by massive increases in plasma catecholamines. In contrast, 80-dB noise in Mg-0 provoked a massive increase in plasma catecholamines (P < 0.001). However, gross pulmonary pathology developed only in Mg-0-shocked rats, not Mg-150-shocked animals. The study provides no evidence for a role of catecholamines in the pathogenesis of Mg-0 shock. The weanling rat displayed the ability to release massive quantities of three catecholamines during the final stages of acute magnesium deficiency and to normalize the plasma catecholamine levels within 16 h after seizure shock.

KEY WORDS: • magnesium deficiency • catecholamines • rats • shock

¹ This work was supported by the Human Genetics Branch, NICHD, NIH, and by Upjohn Diagnostics, the Upjohn Co., Kalamazoo, MI.

² Institutional approvals for publication: Nov. 21 and Dec. 5, 1985. Experiment 1 was abstracted in Pediatr. Res. 16:1063, 1982.

³ Address for reprint requests: Joan L. Caddell, HGB, NICHD, Building 10 8 C-429, The National Institutes of Health, Bethesda, MD 20892. Telephone at NIH: 301-496-1998

⁴ Present address of Deborah Proxmire: 5 Mahler Court, Appleton, WI 54915.

Manuscript received 3 April 1986. Revision accepted 22 May 1986.