Parathyroid hormone secretion and target organ response in experimental acute pancreatitis
P. P. Schachter, M. D. Christy, B. Lobaugh and G. S. Leight Jr
Department of Surgery, Duke University Medical Center, Durham, NC 27710.
To determine changes in parathyroid hormone secretion and target organ
response caused by acute pancreatitis before the development of systemic
toxic conditions, experimental acute pancreatitis was induced in rats with
a choline-deficient, ethionine-supplemented diet. After 7 days, the rats
were weighed and bled, and one kidney was assayed for 25-hydroxyvitamin D1
hydroxylase activity. Several manifestations of pancreatitis were observed
in rats given the diet: weight loss (from 29.6 to 26.3 g vs that for
control rats, from 29 to 52.8 g) and lower dietary intake (15.5 vs 47 g per
rat per 7 days). Serum amylase levels fell from 1794 to 350 U/L in rats
given the choline-deficient, ethionine-supplemented diet compared with
levels of 1800 to 2100 U/L in control rats. The pancreases of rats given
the choline-deficient, ethionine-supplemented diet showed degeneration,
necrosis, and hemorrhaging. Serum levels of calcium, phosphorus, chloride,
and parathyroid hormone did not change significantly throughout the
experiment. Renal 25-hydroxyvitamin D1 hydroxylase activity was higher than
in control rats (8.9 +/- 0.8 vs 7.6 +/- 0.6 fmol/mg of kidney per minute).
Acute pancreatitis in this experimental animal model does not alter serum
levels of calcium and parathyroid hormone or reduce target organ
responsiveness to the hormone.