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Role of mast cells in ischemia/reperfusion‐induced arteriolar endothelium‐dependent vasodilatory dysfunction.
Author(s) -
Dai Hongyan,
Kalogeris Theodore,
Korthuis Ronald
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.762.24
Subject(s) - degranulation , mast cell , vasodilation , acetylcholine , intravital microscopy , ischemia , endothelium , medicine , chemistry , pharmacology , microcirculation , immunology , receptor
The aim of this study was to determine whether ischemia/reperfusion (I/R)‐induced mast cell degranulation plays a role in the development of postischemic arteriolar endothelium‐dependent vasodilator dysfunction. To address this issue, vasodilatory responses to acetylcholine or nitroprusside were monitored in rat mesenteric arterioles (30 um diameter) under control conditions (no ischemia) and following 20 min of ischemia and 60 min of reperfusion using intravital microscopy. The mesentery was superfused during reperfusion with the mast cell stabilizers. Mast cell degranulation was monitored by use of ruthenium red staining. I/R was associated with mast cell degranulation and a marked reduction in vasodilator responses to acetylcholine, but not to nitroprusside. Treatment with mast cell stabilizers prevented mast cell degranulation and improved arteriolar responses to acetylcholine. Moreover, superfusing the mesentery with compound 48/80, at doses that produced a similar degree of mast cell degranulation as noted during I/R, produced a similar deficit in arteriolar endothelium vasodilator responses. Our results are consistent with the concept that postischemic arteriolar endothelium‐dependent vasodilator dysfunction occurs by a mast cell‐dependent mechanism. This work was supported by HL‐082816 from the NIH.