Spinal cord injury: effect of thyrocalcitonin on calcium, magnesium and phosphorus in paraplegic rats.
Calcium, magnesium and phosphorus balances were studied in 20 paraplegic rats (T5) fed ad libitum an 18% casein diet. Ten of the paraplegic animals were treated daily with 4MRC (Medical Research Council) units of thyrocalcitonin. Ten sham-operated rats served as controls. Spinal cord transection caused an immediate increase in urinary excretion of calcium, 550 +/- 70 micrograms/24 hr, compared with controls levels, 257 +/- 85 micrograms/24 hr. Paraplegia also resulted in an elevated excretion of fecal calcium, 39 +/- 5 mg/24 hr, phosphorus, 42 +/- 7 mg/24 hr, and magnesium, 4.6 +/- 0.8 mg/24 hr, compared with that of controls, 26 +/- 6 mg/24 hr, 32 +/- 6 mg/24 hr and 2.7 +/- 0.8 mg/24 hr for calcium, phosphorus and magnesium, respectively. Administration of thyrocalcitonin to paraplegic rats further increased urinary excretion of calcium, 835 +/- 186 micrograms/24 hr. However, fecal losses of calcium, 19 +/- 5mg/24 hr, phosphorus, 31 +/- 6mg/24 hr, and magnesium, 2.6 +/- 0.4mg/24 hr, which were elevated following spinal cord transection, were markedly reduced after thyrocalcitonin treatment. As a result, balances of these compounds, which were depressed in rats following spinal cord transection, were "normalized" after treatment with thyrocalcitonin. It would seem, therefore, worthwhile to study the effect of thyrocalcitonin in spinal cord injured humans in an effort to determine whether or not it would be helpful in improving mineral balances.
D000818:Animals; D002116:Calcitonin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D005243:Feces / Q000032:analysis; D008274:Magnesium / Q000378:metabolism*; D008297:Male; D010264:Paraplegia / Q000209:etiology / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism*; D051381:Rats; D013119:Spinal Cord Injuries / Q000150:complications / Q000378:metabolism*
D010758:Phosphorus; D002116:Calcitonin; D008274:Magnesium; D002118:Calcium