Literature DB >> 2580033

Soft tissue calcium and magnesium content in acute pancreatitis in the dog: calcium accumulation, a mechanism for hypocalcemia in acute pancreatitis.

S K Bhattacharya, R W Luther, J W Pate, A J Crawford, O F Moore, J A Pitcock, G M Palmieri, L G Britt.   

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 translocation of calcium from extracellular to intracellular compartments could play a role in hypocalcemia 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 histologic 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Entities:  

Mesh:

Substances:

Year:  1985        PMID: 2580033

Source DB:  PubMed          Journal:  J Lab Clin Med        ISSN: 0022-2143


  5 in total

1.  Ionized calcium, parathormone, and mortality in critically ill surgical patients.

Authors:  K W Burchard; D S Gann; J Colliton; J Forster
Journal:  Ann Surg       Date:  1990-10       Impact factor: 12.969

2.  Hypocalcemia in experimental pancreatitis occurs independently of changes in serum nonesterified fatty acid levels.

Authors:  D W Rattner; L M Napolitano; J Corsetti; C Compton; G G Stanford; A L Warshaw; B Chernow
Journal:  Int J Pancreatol       Date:  1990-06

Review 3.  Overview of exocrine pancreatic pathobiology.

Authors:  Arun R Pandiri
Journal:  Toxicol Pathol       Date:  2013-11-03       Impact factor: 1.902

4.  Pansteatitis and severe hypocalcaemia in a cat.

Authors:  Eric Zini; Beat Hauser; Pete Ossent; Renate Dennler; Tony M Glaus
Journal:  J Feline Med Surg       Date:  2006-12-18       Impact factor: 2.015

5.  Hypocalcemic tetany: a simple bedside marker of poor outcome in acute pancreatitis.

Authors:  Puneet Chhabra; Surinder S Rana; Vishal Sharma; Ravi Sharma; Deepak K Bhasin
Journal:  Ann Gastroenterol       Date:  2016 Apr-Jun
  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.