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Intraperitoneal free fatty acids induce severe hypocalcemia in rats: A model for the hypocalcemia of pancreatitis

1990; Oxford University Press; Volume: 5; Issue: 12 Linguagem: Inglês

10.1002/jbmr.5650051210

1523-4681

Mark A. Dettelbach, Leonard J. Deftos, Andrew F. Stewart,

Gastroesophageal reflux and treatments

Abstract Indirect evidence suggests a causative role for intraperitoneal free fatty acids (FFA) in hypocalcemia associated with pancreatitis. We examined the effects of intraperitoneal injection of four naturally occurring FFAs on serum calcium in rats. Two saturated FFAs, stearate and palmitate, induced little or no hypocalcemia. Two unsaturated FFAs, oleate and linoleate, caused dramatic hypocalcemia in treated versus control rats (6.3 ± 1.4 and 5.3 ± 0.7 mg/dI, respectively, versus 10.1 ± 0.6). Dose-response studies demonstrated that minute quantities of oleate (100 μl per 250 g rat) caused marked hypocalcemia (7.2 ± 0.3 mg/dI). Treated versus control rats also revealed a decrease in ionized calcium (3.15 ± 0.2 versus 5.6 ± 0.05 mg/dI) and magnesium (1.4 ± 0.15 versus 2.0 ± 0.10), an appropriate increase in PTH levels (1670 ± 451 versus 396 ± 235 pg/ml), and a fall in calcitonin levels (70.4 ± 21.3 versus 47.5 ± 16.4 pg/ml) but no change in albumin or phosphate levels. In vitro, the Ksp of calcium dioleate was shown to be 5.3 × 10-−8 m3/liter3; thus under physiologic conditions 100 μl oleate binds 7.2 mg calcium, or approximately twice the total ECF ionized calcium in the rat. The amounts of intraperitoneal FFA that can easily be achieved in pancreatitis complex pathophysiologically significant amounts of calcium and may lead to severe hypocalcemia.