作者: David W. Rattner , Gregory G. Stanford , Carolyn Compton , Andrew L. Warshaw , John Corsetti
DOI: 10.1007/BF02924404
关键词: Pancreatic disease 、 Glycodeoxycholic acid 、 Internal medicine 、 Calcium metabolism 、 Pancreatitis 、 NEFA 、 Acute pancreatitis 、 Ceruletide 、 Pancreatic duct 、 Endocrinology 、 Medicine
摘要: Hypocalcemia and lipid abnormalities commonly occur in acute pancreatitis. Experimentally, increased plasma concentrations of free fatty acids (NEFA) can lower the serum calcium (Ca). We hypothesized that changes blood-ionized might parallel NEFA concentration This hypothesis was tested a model severe necrotizing pancreatitis mild edematous Adult male Sprague-Dawley rats (300-400 g) were randomized to receive: 100 microL sodium glycodeoxycholic acid (GDOC 34 mmol/L) infused into pancreatic duct produce (Group 1); 0.9% NaCl (NS) 2); Sham laparotomy 3); A 6 h IV infusion cerulein (5 mucg/kg/h) 4); NS 5). significant time dependent decrease Ca concentration, compared normal rats, observed both GDOC-pancreatitis (0.836 +/- .057 vs 1.069 .038 mmol/L p less than 0.001) (0.988 .028 0.05), which maximal 24 after induction The degree hypocalcemia correlated with severity 0.836 0.988 .001). not any control groups. All experimental groups had significantly baseline (p 0.001); however, no further increase occurred conjunction time-dependent decline ionized concentrations. Although these experiments comparable those measured human (exclusive hyperlipemic pancreatitis), course suggests increases are primary factor mediating hypocalcemia.