Soft tissue calcium and magnesium content in acute pancreatitis in the dog

Calcium accumulation, a mechanism for hypocalcemia in acute pancreatitis

Syamal Bhattacharya, R. Wayne Luther, James W. Pate, Alice J. Crawford, O. Fred Moore, James A. Pitcock, Genaro M.A. Palmieri, Louis G. Britt

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

The mechanism of hypocalcemia in acute pancreatitis remains unknown despite continued investigative work over the past several decades. Because acute pancreatitis is accompanied by multiple systemic manifestations and alterations of plasma membranes, the possibility that an abnormal transtocation of calcium from extracellular to intracellular compartments could play a role in hypocalcemla of acute pancreatitis was investigated in dogs. Acute pancreatitis was induced by injecting bile into the pancreatic duct. Plasma calcium, magnesium, and amylase concentrations were determined. Calcium and magnesium contents were also measured in biopsy specimens of pancreas, liver, skeletal muscle, and kidney before and after induction of acute pancreatitis. As expected, hypocalcemia and hyperamylasemia occurred 6 hours after induction of pancreatitis, and persisted throughout the experiment, 13 to 25 hours. Plasma magnesium concentration fell at 6 and 18 hours, and returned to an almost normal level by the end of the study. A significant elevation in calcium content of pancreas (71%), liver (24%). and muscle (112%), and 25% reduction of calcium in kidney were observed in dogs with histologic signs of pancreatitis. However, tissue magnesium concentration fell in pancreas (18%) but remained unchanged in the other tissues investigated. No significant changes in any variables were detected in sham-operated animals. In another group of dogs in which the accessory pancreatic duct was not occluded when bile was injected, the histologie lesions were extremely mild, although the plasma calcium concentration and the pancreatic calcium and magnesium contents were altered just as much as in the severely affected dogs. Data suggest that the hypocalcemia of acute pancreatitis may be the result, at least in part, of accumulation of calcium in soft tissues. The decreased calcium content in kidney could be related to hypocalcemia. Because calcium content in pancreas was uniformly elevated in animals with severe and mild pancreatitis, we postulate that calcium accumulation in acute pancreatitis is not solely the result of necrosis but is an early biochemical event in the pathogenesis of systemic manifestations of this disorder. Abnormally high levels of circulating pancreatic enzymes such as amylase and lipase may cause widespread plasma membrane alterations, thus stimulating significant calcium accumulation in distant soft tissues, especially in muscle.

Original languageEnglish (US)
Pages (from-to)417-421
Number of pages5
JournalThe Journal of Laboratory and Clinical Medicine
Volume105
Issue number4
StatePublished - Jan 1 1985

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Hypocalcemia
Pancreatitis
Magnesium
Dogs
Tissue
Calcium
Pancreas
Muscle
Pancreatic Ducts
Cell membranes
Amylases
Kidney
Plasmas
Bile
Liver
Ducts
Animals
Cell Membrane
Hyperamylasemia
Muscles

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine

Cite this

Soft tissue calcium and magnesium content in acute pancreatitis in the dog : Calcium accumulation, a mechanism for hypocalcemia in acute pancreatitis. / Bhattacharya, Syamal; Luther, R. Wayne; Pate, James W.; Crawford, Alice J.; Moore, O. Fred; Pitcock, James A.; Palmieri, Genaro M.A.; Britt, Louis G.

In: The Journal of Laboratory and Clinical Medicine, Vol. 105, No. 4, 01.01.1985, p. 417-421.

Research output: Contribution to journalArticle

Bhattacharya, Syamal ; Luther, R. Wayne ; Pate, James W. ; Crawford, Alice J. ; Moore, O. Fred ; Pitcock, James A. ; Palmieri, Genaro M.A. ; Britt, Louis G. / Soft tissue calcium and magnesium content in acute pancreatitis in the dog : Calcium accumulation, a mechanism for hypocalcemia in acute pancreatitis. In: The Journal of Laboratory and Clinical Medicine. 1985 ; Vol. 105, No. 4. pp. 417-421.
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AU - Crawford, Alice J.

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