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Biomedical subjects

W H Bergstrom

Publications and source records attributed to W H Bergstrom.

15 recordsLinked to original sources

Pineal and adrenal effects on calcium homeostasis in the rat.

In human infants and newborn rats, white light at the intensity used to treat hyperbilirubinemia lowers serum calcium concentration. Occipital shielding or (in newborn rats) exogenous melatonin prevents this effect. Propranolol, by inhibiting melatonin synthesis, also causes hypocalcemia, which is preventable by melatonin. Metyrapone or adrenalectomy prevents hypocalcemia after light exposure or propranolol. Exogenous corticosterone lowers serum calcium; this is prevented by supplementary melatonin. In adult rats, the change in calcium after light, propranolol, or corticosterone is minimal. After parathyroidectomy or a diet with a high calcium/low phosphorus ratio, the hypocalcemic effect of these three agents is restored. Bone samples removed after light exposure or corticosterone administration show increased calcium uptake; this is blocked by supplementary melatonin in vivo or by addition of melatonin to the incubation medium. We postulated that the hypocalcemic effect of light or propranolol was due to an acute increase in corticosterone-mediated bone calcium uptake when circulating melatonin was decreased by reduction of the rate of melatonin synthesis. In our study, pinealectomized rats showed no change in serum calcium after light or propranolol; their hypocalcemic response to corticosterone was greater than that of sham-operated controls. Exogenous parathyroid hormone prevented light-induced hypocalcemia in newborn rats.

Adrenal Glands

Calcemic responses to photic and pharmacologic manipulation of serum melatonin.

Phototherapy of newborn rats (NBR) resulted in a decrease in serum calcium and melatonin levels. Transcranial light penetrance in NBR increased with wavelength. Below 640 nm (penetrance = 6.9%), no hypocalcemic effect could be demonstrated. Shielding the occiput of NBR prevented a decrease in serum calcium during phototherapy and substantially reduced the decrease in melatonin found in unshielded NBR. Intraperitoneal injection of propranolol, an inhibitor of melatonin synthesis, caused a decrease in serum calcium in shaded NBR. In contrast, when melatonin was injected with propranolol a decrease in serum calcium did not occur. Additionally, intraperitoneal isoproterenol before phototherapy protected against a decrease in serum calcium. These data are consistent with an hypothesis that a decrease in serum calcium during phototherapy results from transcranial photic inhibition of melatonin synthesis.

Animals

Effect of hyperventilation on total calcium, ionized calcium, and serum phosphorus in neonates.

The effect of alkalosis (pH greater than 7.55) on total calcium, ionized calcium, and serum phosphorus was studied in seven infants with persistent pulmonary hypertension (PPH) before, during, and after hyperventilation. Hyperventilation-induced alkalosis resulted in marked decreases in total calcium, phosphorus, and ionized calcium. There was an inverse correlation between plasma Ca+2 and pH; a 0.1-unit increase in blood pH decreased Ca+2 by 0.42 mg/dl. Two of the study infants had ionized calcium concentrations less than 2.5 mg/dl during hyperventilation. These disturbing changes in total calcium, ionized calcium, and serum phosphorus could have potentially detrimental effects on neonates with PPH.

Alkalosis

Bone changes induced by diphenylhydantoin in chicks on a controlled vitamin D intake.

Florid rickets developed in chicks receiving doses of diphenylhydantoin analogous to doses used in humans as anticonvulsants, vitamin D3 being given in amounts sufficient for normal bone mineralization in controls. The changes in the bones were directly related to the dose of diphenylhydantoin and inversely related to the dose of vitamin D3. Bone mineralization was assessed by roentgenography, histological examination, microradiography, and measurement of bone ash. Of these methods, roentgenography was the least sensitive. Rachitic changes were detectable by light microscopy and microradiography in chicks whose skeletons appeared normal roentgenographically. Roentgenographic evidence of rickets became detectable only when the rickets was far advanced. Rickets developed at serum levels of diphenylhydantoin similar to those found in patients taking anticonvulsant medication.

Animals

Prophylaxis against hypocalcemia in low-birth-weight infants requiring bicarbonate infusion.

Forty-eight low-birth-weight infants with varying degrees of respiratory distress were studied with respect to serum calcium concentration and urinary calcium excretion. Serum calcium decreased over the 24-hour study period in infants who did not receive calcium infusion. The decrease was greater in those receiving bicarbonate therapy for acidosis. Continuous calcium infusion at 1 mg/kg/hr sustained relatively normal serum calcium concentration, even in those infants who required bicarbonate. Since the changes in estimated extracellular calcium could not be accounted for by urinary excretion, a shift of calcium into bone was postulated.

Bicarbonates

Diphenylhydantoin: effects on calcium metabolism in the chick.

Rickets, hypocalcemia, decreased duodenal calcium transport, and reduction of calcium binding protein have been produced in chicks treated with diphenylhydantoin. These effects are directly related to diphenylhydantoin dose and inversely related to the intake of vitamin D(3) (cholecalciferol).

Animals