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Cell wounding in early experimental acute pancreatitis
Dale E Bockman1, Junchao Guo, Michael W Müller
1Department of General Surgery, University of Heidelberg, Germany. hodney@msn.com
Laboratory Investigation; a Journal of Technical Methods and Pathology
|February 10, 2004
Summary
Acute pancreatitis may begin with damage to the cell membrane, allowing substances to enter acinar cells. This study shows caerulein induces membrane damage, potentially initiating pancreatitis.
Area of Science:
- Cell Biology
- Gastroenterology
- Pathophysiology
Background:
- Cell membrane damage allows abnormal substance transmission into the cytosol.
- Albumin penetration into acinar cells suggests early membrane damage in acute pancreatitis.
Purpose of the Study:
- To investigate if direct cell membrane damage is a key factor in acute pancreatitis induction.
- To determine if cell membrane damage alters the balance of extra- and intracellular substances.
Main Methods:
- Administered fluorescein-dextran with supramaximal caerulein doses intravenously or directly into the pancreas.
- Observed tracer penetration patterns: cytosolic and vesicular/vacuolar.
Main Results:
- Fluorescein-dextran rapidly penetrated acinar cell cytosol within 10 minutes after intravenous administration with caerulein.
- Strong cytoplasmic fluorescence was observed within 5 minutes after direct pancreatic injection.
Conclusions:
- Supramaximal caerulein in vivo damages acinar cell membranes, permitting large molecules to enter the cytosol.
- This membrane damage may lead to abnormally high intracellular concentrations of Ca(2+) and other substances, initiating pancreatitis.
- The findings suggest membrane wounding could initiate human pancreatitis.