New pharmacological approaches to the prevention of myocardial ischemia-reperfusion injury

Kai Yee Chin, Chengxue Qin, Lauren May, Rebecca H. Ritchie, Owen L. Woodman

Research output: Contribution to journalReview ArticleResearchpeer-review

Abstract

Background: Early reperfusion of the blocked vessel is critical to restore the blood flow to the ischemic myocardium to salvage myocardial tissue and improve clinical outcome. This reperfusion strategy after a period of ischemia, however, may elicit further myocardial damage named myocardial reperfusion injury. The manifestations of reperfusion injury include arrhythmias, myocardial stunning and micro-vascular dysfunction, in addition to significant cardiomyocyte death. It is suggested that an overproduction of reactive oxygen species, intracellular calcium overload and inflammatory cell infiltration are the most important features of myocardial ischemia-reperfusion injury. Objective: In this review, various pharmacological interventions to treat myocardial reperfusion injury including the antioxidant flavonols, hydrogen sulfide, adenosine, opioids, incretin-based therapies and cyclosporin A which targets the mitochondrial permeability transition pore are discussed. Conclusion: The processes involved in reperfusion injury might provide targets for improved outcomes after myocardial infarction but thus far that aim has not been met in the clinic.

Original languageEnglish
Pages (from-to)1689-1711
Number of pages23
JournalCurrent Drug Targets
Volume18
Issue number15
DOIs
Publication statusPublished - 1 Jan 2017

Keywords

  • Adenosine
  • Antioxidant
  • Cardioprotection
  • Cyclosporin A
  • Flavonol
  • Hydrogen sulfide
  • Incretin-based therapies
  • Ischemia-reperfusion
  • Opioids
  • Reactive oxygen species

Cite this

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title = "New pharmacological approaches to the prevention of myocardial ischemia-reperfusion injury",
abstract = "Background: Early reperfusion of the blocked vessel is critical to restore the blood flow to the ischemic myocardium to salvage myocardial tissue and improve clinical outcome. This reperfusion strategy after a period of ischemia, however, may elicit further myocardial damage named myocardial reperfusion injury. The manifestations of reperfusion injury include arrhythmias, myocardial stunning and micro-vascular dysfunction, in addition to significant cardiomyocyte death. It is suggested that an overproduction of reactive oxygen species, intracellular calcium overload and inflammatory cell infiltration are the most important features of myocardial ischemia-reperfusion injury. Objective: In this review, various pharmacological interventions to treat myocardial reperfusion injury including the antioxidant flavonols, hydrogen sulfide, adenosine, opioids, incretin-based therapies and cyclosporin A which targets the mitochondrial permeability transition pore are discussed. Conclusion: The processes involved in reperfusion injury might provide targets for improved outcomes after myocardial infarction but thus far that aim has not been met in the clinic.",
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New pharmacological approaches to the prevention of myocardial ischemia-reperfusion injury. / Chin, Kai Yee; Qin, Chengxue; May, Lauren; Ritchie, Rebecca H.; Woodman, Owen L.

In: Current Drug Targets, Vol. 18, No. 15, 01.01.2017, p. 1689-1711.

Research output: Contribution to journalReview ArticleResearchpeer-review

TY - JOUR

T1 - New pharmacological approaches to the prevention of myocardial ischemia-reperfusion injury

AU - Chin, Kai Yee

AU - Qin, Chengxue

AU - May, Lauren

AU - Ritchie, Rebecca H.

AU - Woodman, Owen L.

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Background: Early reperfusion of the blocked vessel is critical to restore the blood flow to the ischemic myocardium to salvage myocardial tissue and improve clinical outcome. This reperfusion strategy after a period of ischemia, however, may elicit further myocardial damage named myocardial reperfusion injury. The manifestations of reperfusion injury include arrhythmias, myocardial stunning and micro-vascular dysfunction, in addition to significant cardiomyocyte death. It is suggested that an overproduction of reactive oxygen species, intracellular calcium overload and inflammatory cell infiltration are the most important features of myocardial ischemia-reperfusion injury. Objective: In this review, various pharmacological interventions to treat myocardial reperfusion injury including the antioxidant flavonols, hydrogen sulfide, adenosine, opioids, incretin-based therapies and cyclosporin A which targets the mitochondrial permeability transition pore are discussed. Conclusion: The processes involved in reperfusion injury might provide targets for improved outcomes after myocardial infarction but thus far that aim has not been met in the clinic.

AB - Background: Early reperfusion of the blocked vessel is critical to restore the blood flow to the ischemic myocardium to salvage myocardial tissue and improve clinical outcome. This reperfusion strategy after a period of ischemia, however, may elicit further myocardial damage named myocardial reperfusion injury. The manifestations of reperfusion injury include arrhythmias, myocardial stunning and micro-vascular dysfunction, in addition to significant cardiomyocyte death. It is suggested that an overproduction of reactive oxygen species, intracellular calcium overload and inflammatory cell infiltration are the most important features of myocardial ischemia-reperfusion injury. Objective: In this review, various pharmacological interventions to treat myocardial reperfusion injury including the antioxidant flavonols, hydrogen sulfide, adenosine, opioids, incretin-based therapies and cyclosporin A which targets the mitochondrial permeability transition pore are discussed. Conclusion: The processes involved in reperfusion injury might provide targets for improved outcomes after myocardial infarction but thus far that aim has not been met in the clinic.

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KW - Antioxidant

KW - Cardioprotection

KW - Cyclosporin A

KW - Flavonol

KW - Hydrogen sulfide

KW - Incretin-based therapies

KW - Ischemia-reperfusion

KW - Opioids

KW - Reactive oxygen species

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