title: Myocardial ischaemia and reperfusion injury: reactive oxygen species and the role of neutrophil.
abstract: A growing body of evidence suggests that oxygen radicals can mediate myocardial tissue injury during ischaemia and, in particular, during reperfusion. This review focuses on the role of neutrophil as a mediator of myocardial damage. Upon reperfusion, neutrophils accumulate and produce an inflammatory response in the myocardium that is responsible, in part, for the extension of tissue injury associated with reperfusion. It has shown that the inhibition of neutrophil accumulation and adhesion is associated with decreased infarct size. This strongly suggests that myocardial cells at risk region undergo irreversible changes upon reperfusion and accumulation of neutrophils. Several pharmacological agents (ibuprofen, allopurinol, prostacyclin, and prostaglandin E analogues) protect the myocardium from reperfusion injury. In addition, the mechanisms by which these agents act and directions of research that may lead to therapeutically useful approaches are also discussed in this review.
authors.affiliation: Dr. Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical Sciences, University of Karachi, Karachi-75270, Pakistan. arshad.saeed@iccs.edu
authors.forename: Sheikh Arshad
authors.initials: SA
authors.lastname: Saeed
authors.forename: Muhammad Anwar
authors.initials: MA
authors.lastname: Waqar
authors.forename: Akbar Jaleel
authors.initials: AJ
authors.lastname: Zubairi
authors.forename: Hadi
authors.initials: H
authors.lastname: Bhurgri
authors.forename: Abdullah
authors.initials: A
authors.lastname: Khan
authors.forename: Saqib Ali Sikander
authors.initials: SA
authors.lastname: Gowani
authors.forename: Saima N
authors.initials: SN
authors.lastname: Waqar
authors.forename: M Iqbal
authors.initials: MI
authors.lastname: Choudhary
authors.forename: Saima
authors.initials: S
authors.lastname: Jalil
authors.forename: Ali Hyder
authors.initials: AH
authors.lastname: Zaidi
authors.forename: Iffat
authors.initials: I
authors.lastname: Ara
mesh_terms: D000493:Allopurinol / Q000494:pharmacology; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology; D016166:Free Radical Scavengers / Q000494:pharmacology; D006801:Humans; D007052:Ibuprofen / Q000494:pharmacology; D016285:Iloprost / Q000494:pharmacology; D017202:Myocardial Ischemia / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology* / Q000517:prevention & control; D009504:Neutrophils / Q000502:physiology*; D011459:Prostaglandins E, Synthetic / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000494:pharmacology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016166:Free Radical Scavengers; D011459:Prostaglandins E, Synthetic; D017382:Reactive Oxygen Species; D000493:Allopurinol; D011464:Epoprostenol; D016285:Iloprost; D007052:Ibuprofen