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Articles in PresS, published online ahead of print September 20, 2002
J Appl Physiol, 10.1152/jap.00637.2002
Submitted on July 12, 2002
Accepted on September 6, 2002
1 Department of Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA
* To whom correspondence should be addressed. E-mail: jwood2{at}kumc.edu.
Systemic hypoxia produces an inflammatory response characterized by increases in reactive O2 species (ROS), venular leukocyte-endothelial adherence and emigration, and vascular permeability. Inflammation is typically initiated by mediators released from activated perivascular cells that generate the chemotactic gradient responsible for extravascular leukocyte accumulation. These experiments were directed to study the possible participation of mast cells in hypoxia-induced microvascular inflammation. Mast cell degranulation, ROS levels, leukocyte adherence and emigration, and vascular permeability were studied in the mesenteric microcirculation using intravital microscopy of anesthetized rats. The main findings were: 1. Activation of mast cells with compound 48/80 in normoxia produced microvascular effects similar, but not identical, to those of hypoxia; 2. Systemic hypoxia resulted in rapid mast cell degranulation; 3. Blockade of mast cell degranulation with cromolyn prevented or attenuated the hypoxia-induced increases in ROS, leukocyte adherence/emigration, and vascular permeability; and 4. Mast cell degranulation during hypoxia was prevented by administration of the antioxidant lipoic acid and of nitric oxide (NO). These results show that mast cells play a key role in hypoxia-induced inflammation and suggest that alterations in the ROS/NO balance may be involved in mast cell activation during hypoxia.
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