Mast cells have recently been shown to be activated in reperfused tissue. In the skeletal muscle of the reperfused mouse hind limb, extensive mast cell degranulation has been noted. Use of mast cell-deficient (W/Wv) mice has yielded protection against local and remote reperfusion injury. Mast cells have also been shown to mediate local injury after acid aspiration. Whether mast cells are complement-triggered effectors is uncertain. The mast cell and complement pathways likely augment one another, although evidence is still lacking.
It has been postulated that reperfusion injury could be attenuated by interrupting certain vagal nerve conduction pathway either surgically or pharmacologically because of the proximity of the mast cells to the peripheral nerve endings. Cervically vagotomized mice showed a 90 percent reduction in their remote lung injury and 40 percent reduction in local skeletal injury following hind limb ischemia-reperfusion. Rats treated with a substance P antagonist L-703606, a blocker of the NK1 receptor, have attenuated myocardial injury after ischemia. It is likely that, depending upon the timing of therapy, reperfusion injury would best be treated using a combination of anti-complement and antimast cell agents.
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