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Myocardial infarction and nitric oxide

R J Bing1, H Suzuki

  • 1Department of Experimental Cardiology, Huntington Medical Research Institutes, Pasadena, CA 91101, USA.

Molecular and Cellular Biochemistry
|July 1, 1996
PubMed

Insights

Inducible nitric oxide synthase (iNOS) increases in heart attack tissue, mainly in macrophages. S-methylisothiourea (SMT) most effectively inhibited iNOS in rabbit hearts, while dexamethasone and cyclosporin A did not.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Molecular Biology

Background:

  • Myocardial infarction triggers inflammatory responses in heart muscle.
  • Nitric oxide synthase (NOS) plays a role in cardiovascular function and inflammation.
  • The inducible form (iNOS) is implicated in various disease states.

Purpose of the Study:

  • To investigate the induction of inducible nitric oxide synthase (iNOS) in infarcted heart muscle.
  • To identify the cellular localization of iNOS in myocardial infarction.
  • To evaluate the efficacy of iNOS inhibitors in this context.

Main Methods:

  • Induction of myocardial infarction by coronary artery ligation in rabbits.
  • Immunohistochemical analysis for iNOS expression.
  • Administration of specific iNOS inhibitors: S-methylisothiourea (SMT), dexamethasone, and cyclosporin A.
  • Assessment of macrophage apoptosis.

Main Results:

  • Significant increase in iNOS in infarcted rabbit heart muscle starting on day three post-ligation.
  • iNOS was primarily localized in macrophages in both rabbit and human myocardial infarction samples.
  • S-methylisothiourea (SMT) demonstrated the most potent inhibition of iNOS, particularly in non-infarcted areas.
  • Dexamethasone and cyclosporin A failed to inhibit iNOS.
  • Macrophage apoptosis was observed two days after coronary artery ligation.

Conclusions:

  • iNOS is significantly induced in macrophages within infarcted heart tissue.
  • SMT shows potential as an iNOS inhibitor in myocardial infarction, though its effect is more pronounced in healthy tissue.
  • Standard immunosuppressants like dexamethasone and cyclosporin A are ineffective against iNOS in this model.
  • Macrophage apoptosis is an early event following myocardial infarction.

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