Nutritional Secondary Hyperparathyroidism in the Horse

72 Expcrimcntal Nutritional Sccondary Hypcrparathyroidism in the Horse. . .
It would seem, therefore, that an inverse relationship between
calcium and phosphorus should not exist. An experiment by MCLEAN
et al. (1946) offered the explanation. They introduced the term “biological
solubility” and defined undersaturation, saturation, and supersaturation
of calcium and phosphorus in blood serum on the basis of
this term. “The limit of biological solubility is the point at which
deposition of the bone salt just occurs in the matrix of rachitic cartilage
in vitro.” Levels above this point were considered supersaturated and
below this level undersaturated. MCLEAN et al. performed the following
experiment: Adult dogs whose serum did not mineralize rachitic
cartilage in vitro were given a large dose of parathormone at 0 and at
4 hours. The serum calcium rose rapidly and leached maximum level
after 12 hours. A concurrent but slight rise in the serum phosphorus
level was also recorded. At 4 hours the serum induced a slight mineralization
of rachitic cartilage in vitro. After 8 hours the ion product of
calcium and phosphorus of blood serum and in vitro mineralization
tendency was still higher. They concluded, then, that at 4 hours the
serum must have been at least saturated and, after 8 hours, supersaturated.
According to these authors, the cause of supersaturation
must be sought in the active intervention by the parathyroid hormone
because “there is no way in which a solution of a salt, in contact with
a solid phase, may become supersaturated by simple equilibrium with
the solid”.
The reports just mentioned concerned the interrelationship
between calcium and phosphorus in noncompensatory, exogenous
hyperparathyroidism. The results indicate, therefore, the effects of the
parathyroid hormone on serum calcium and phosphorus. The interrelationship
between calcium and phosphorus can be better demonstrated
in the reverse condition, viz., the effect of different levels of
serum calcium and phosphorus on the parathyroid glands. HAM et al.
(1 940) showed conclusively that “hypocalcemia, instead of hyperphosphatemia,
is the primary cause of physiological hypertrophy of
the parathyroid glands”. Their results were confirmed by PATT and
LUCKIIARUT (1942), STOERK and CARNES (1945), and EWGFELDT et al.
(1954). Different ways have been employed to produce hypocalcemia
leading to secondary hyperparathyroidism. I-IAM et al. simply underfed
calcium to induce hypocalcemia, PATT and LUCKHARUT lowered serum
calcium by intravenous injections of sodium oxalate, and COPP et al.
(1962) used EDTA injections. With all these methods serum calcium
alone was influenced, and regardless of the method the result was, as far
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