title: Resident cardiac mast cells and ischemia-reperfusion injury.
abstract: 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 modern 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.
  
  
  METHODS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India. manjeet@Pbi.Ernet.in
authors.forename: Manjeet
authors.initials: M
authors.lastname: Singh
authors.forename: Harjot K
authors.initials: HK
authors.lastname: Saini
mesh_terms: D018674:Adrenergic Antagonists / Q000627:therapeutic use; D017209:Apoptosis; D002118:Calcium / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D019157:Ischemic Preconditioning, Myocardial; D008407:Mast Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology* / Q000517:prevention & control; D009569:Nitric Oxide / Q000378:metabolism; D010726:Phosphodiesterase Inhibitors / Q000627:therapeutic use; D011969:Receptors, Histamine H1 / Q000187:drug effects; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D018674:Adrenergic Antagonists; D018836:Inflammation Mediators; D010726:Phosphodiesterase Inhibitors; D011969:Receptors, Histamine H1; D009569:Nitric Oxide; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D002118:Calcium