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Resident Cardiac Mast Cells and Ischemia-Reperfusion Injury
Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India Background: The intense inflammatory reaction following reperfusion of ischemic myocardium has been implicated as a factor in the extension of myocardial injury. One of the therapeutic goals of modem cardiology is to design strategies to limit the infarct size following myocardial infarction. A sound understanding of the inflammatory cascade that involves the release of various proinflammatory mediators from cardiac cells is necessary before a specific intervention is pursued.Observation: Summarized is the role of resident cardiac mast cells, which are noted to release inflammatory mediators, in ischemia-reperfusion-induced myocardial injury. Various pharmacologic interventions, such as disodium cromoglycate and ketotifen, that stabilize cardiac mast cells, or agents such as chlorpheniramine and cetirizine that prevent their degranulation during ischemia and reperfusion, may prove to be potential therapeutic agents to limit or salvage ischemia-reperfusion-induced injury.Conclusion: On the basis of the effects of histamine H1 antagonists, adrenoceptor blockers, cellular calcium and nitric oxide modulators, as well as inhibitors of phosphodiesterase and mitogen-activated protein kinase on mast cells, cardiac resident mast cells may represent a novel target for the development of cardioprotective agents.
Key Words: cardiac mast cells • ischemia-reperfusion injury • preconditioning, nitric oxide • cellular calcium • p38 mitogen-activated protein kinase • phosphodiesterase
Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 8, No. 2,
135-148 (2003) This article has been cited by other articles:
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