Gamble, Ross, and Tisdall (1) originally pointed out that electrolytes and water were lost from the body during fasting in a manner which could be reasonably predicted from the concentration of salts in the body fluids. This concept is the basis for the study of changes in body composition by examination of electrolyte balance and weight changes. Darrow, Da Silva, and Stevenson (2) elaborated the method of calculation and showed that shifts of sodium between extracellular and intracellular fluid could be inferred in certain conditions from balance measurements. In this laboratory, studies in both man and animals (3, 4) have frequently demonstrated losses or gains of sodium which cannot be reasonably explained on the basis of shifts so calculated. Two possible explanations are: (a) Unmeasured skin losses may lead to the calculation of erroneously large retentions, or (b) Electrolyte may be sequestered in the body in an osmotically inactive form quickly available to the body fluids. Flanagan, Davis, and Overman (5), studying both balances and composition of tissues in dogs with adrenal insufliciency, noted such discrepancies and suggested that bone might serve as a sodium reservoir.The early work of Gabriel (6) demonstrated the presence of substantial amounts of sodium in the chloride-free residue of bone extracted with alkaline glycol solutions. Harrison, Darrow, and Yannet (7) showed that the ratio of sodium to chlonde in the skeleton is greatly in excess of that found in a plasma ultrafiltrate, and defined this as "extra" bone sodium. Subsequent investigators have confirmed these findings (8, 9), and Kaltreider, Meneely, Allen, and Bale (8), Stern, Cole, Bass, and

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ABSTRACT. Metabolic investigations, including the use of stable isotopes of calcium, were used to study calcium kinetics in three children with the hyperprostaglandin E syndrome. The studies were performed both during indomethacin treatment and in the absence of therapy. Off therapy, each child had hypercalciuria (mean urinary calcium excretion 0.478 mM/kg/d), hyperprostaglandinuria, and elevated serum calcitriol concentration. All had diminished bone density and were euparathyroid. Indomethacin treatment was associated with a marked reduction in serum calcitriol concentration, as well as decreased prostaglandin E excretion. Mean urinary calcium excretion fell to 0.135 mM/kg/d. The stable isotope studies defined two components to the hypercalciuria of this disease: an indomethacin-sensitive dietary contribution and a relatively indomethacin-resistant bone resorptive element. Bone densitometry confirmed the presence of the resorptive element by demonstrating skeletal demineralization. (

ABSTRACT. 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. (Pediatr Res 22: [414][415][416]1987) Abbreviations NBR, newborn rats IP, intraperitoneal CAP, occipital shield Serum calcium concentration decreases in human infants and NBR exposed to white light at the energy level used in phototherapy for hyperbilirubinemia (5 pW/cm2/nm) (I, 2). This effect is not seen when the occiput is shielded (2), when blue light is used (2, 3), or, in NBR, when exogenous melatonin is given before light exposure (2). Transcranial illumination of the pineal inhibits melatonin synthesis (4), and we have hypothesized that the resultant decrease in serum melatonin might be responsible for the hypocalcemic effect of phototherapy (2).If this hypothesis is valid, it should be possible to demonstrate: 1) a relationship between the transcranial penetrance of light and its effect on calcium, 2) decreased serum melatonin concurrent with decreased serum calcium during phototherapy, and 3) changes in serum calcium after pharmacologic manipulation of melatonin synthesis.We determined transcranial light penetrance and serum calcium levels after exposure to light at 510 nm (blue), 545 nm (green), and 640 nm (yellow). We also measured serum melatonin and calcium in NBR during phototherapy with and without CAP; controls were shaded littermates.

When young rats are exposed to white fluorescent light the concentration of calcium in their serum decreases. This effect is prevented by shielding the occiput, by inhibiting corticosterone synthesis, and by exogenous melatonin. Furthermore, the expected hypocalcemic response to cortisol injection is prevented by melatonin. Light-induced hypocalcemia may result from increased calcium uptake by bone when the blocking effect of melatonin decreases after pineal inhibition by transcranial illumination.

Although PEMF's have been found to promote fracture healing and to modulate the activity of bone cells in vitro, effects on bone metabolism are largely unexplored. A bioassay using neonatal rat calvarial bone was used to determine the early effects of a pulsing electromagnetic field (PEMF) exposure in vivo and in vitro on bone metabolic calcium exchange. Bone discs taken from whole body exposed animals (0-4 hours) show a log exposure time-dependent average increase in net Ca uptake in the 0-50% range (r2 = 0.83). This increase could be detected immediately after exposure and also after 24 hours, but not 48 hours later. Animals given whole body PEMF exposure also showed a decrease in serum calcium and did not elevate serum Ca after administration of exogenous parathyroid hormone (PTH). Bone discs from untreated rats, exposed to PEMF for 15 minutes in vitro and then assayed, showed net Ca uptake increases of a similar magnitude and also were refractory to the Ca-releasing effect of PTH. Unexposed discs responded normally to PTH by decreasing net Ca uptake. Treatment of calvarial discs with calcitonin or acetazolamide, both of which inactivate osteoclasts, made the bone refractory to further increases in Ca uptake by PEMF. These results suggest that PEMF exposure produces PTH-refractory osteoclastics and has a relatively rapid effect on increasing net bone Ca uptake, putatively due to a decrease in PTH/paracrine-mediated bone resorption.

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