Therapeutic strategies to reduce TNF-alpha mediated cardiac contractile depression following ischemia and reperfusion.

Recent evidence has implicated proinflammatory mediators such as TNF- alpha in the pathophysiology of ischemia-reperfusion (I/R) injury. Clinically, serum levels of TNF-alpha are increased after myocardial infarction and after cardiopulmonary bypass. Each of these represent clinically relevant instances of cardiac I/R injury. We and others have recently reported that TNF-alpha is produced by the heart following experimental I/R in animals and that TNF-alpha directly decreases animal and human myocardial contractility in a dose dependent fashion. Thus, strategies to reduce or neutralize myocardial TNF- alpha production should conceptually decrease myocardial contractile dysfunction following I/R. The purposes of this manuscript are: 1) to explore the clinical and experimental instances of I/R injury in which TNF-alpha is elevated, 2) to review the molecular mechanisms of TNF- alpha induced contractile dysfunction, 3) to examine both experimental and clinical strategies of reducing myocardial TNF-alpha production, and 4) to determine the influence of reducing post-I/R TNF-alpha on cardiac contractile function in both animals and man.

• Publication year

  1999

• Venue

  Journal of Molecular and Cellular Cardiology

• Publication date

  1999-05-01

• Fields of study

  Medicine

• Identifiers
  DOI 10.1006/JMCC.1999.0924PMID 10336835
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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