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Journal of Histochemistry and Cytochemistry, Vol. 49, 1055-1056, August 2001, Copyright © 2001, The Histochemical Society, Inc.

BRIEF REPORT

Mast Cell Mediation of Muscle and Pulmonary Injury Following Hindlimb Ischemia–Reperfusion

Chandrika Mukundana, Michael F. Gurishc, K. Frank Austenc, Herbert B. Hechtmana, and Daniel S. Friendb
a Departments of Surgery, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
b Pathology, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
c Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts

Correspondence to: Daniel S. Friend, Div. of Rheumatology and Immunology, Smith Building, Rm. 628, One Jimmy Fund Way, Boston, MA 02115.

We have observed extensive mast cell degranulation in the reperfused hindlimb muscle of the mouse, accompanied by pathological changes within the muscle. As quantitated by the tissue:blood 125I permeability ratio, both the hindlimbs and lungs exhibited a significant increment in permeability during hindlimb reperfusion. In lungs of the same mice, mast cell-derived chymase mMCP-1 coats alveolar macrophages, an event noted by us in acid-induced direct lung injury. Mast cells in the lung contain mMCP-1, whereas those in the muscle do not. Neither extensive muscle injury nor an increased pulmonary permeability index occurs in the mast cell-deficient W/Wv mice. We conclude that the mast cell is a key mediator in both local ischemia–reperfusion injury (I–R) of muscle and consequent remote lung injury. (J Histochem Cytochem 49:1055–1056, 2001)

Key Words: ischemia–reperfusion, hindlimb, lung, mast cell


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