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Am J Physiol Gastrointest Liver Physiol 275: G212-G218, 1998;
0193-1857/98 $5.00
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Vol. 275, Issue 2, G212-G218, August 1998

Postischemic inflammation: a role for mast cells in intestine but not in skeletal muscle

Samina Kanwar, Michael J. Hickey, and Paul Kubes

Immunology Research Group, Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada T2N 4N1

The objective of this study was to directly study a role for mast cells in ischemia-reperfusion (I/R)-induced mucosal and microvascular dysfunction. I/R was induced in the intestine and skeletal muscle (gastrocnemius and cremaster muscle) of wild-type mice and mast cell-deficient mice (W/Wv). Changes in mucosal permeability (blood-to-lumen clearance of 51Cr-EDTA), leukocyte infiltration (myeloperoxidase activity in the intestine and intravital microscopy in the cremaster muscle), and vascular permeability (tissue wet-to-dry weight ratio and FITC-albumin leakage) were measured as indexes of tissue dysfunction. In wild-type animals, intestinal I/R induced a significant increase in mucosal permeability, leukocyte infiltration, and vascular permeability. Mast cell-deficient animals were completely protected from I/R-induced mucosal dysfunction. However, skeletal muscle I/R induced a significant increase in leukocyte infiltration, FITC-albumin leakage, and edema formation to the same degree in both wild-type and mast cell-deficient animals. These data suggest that mast cells may be important mediators of I/R-induced mucosal and microvascular dysfunction in the intestine but not of microvascular dysfunction in skeletal muscle.

reperfusion injury; mucosal permeability; leukocyte recruitment


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