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Inducible NO Synthase mRNA Expression and Infiltration of Rats Myocardium with Inflammatory Cells in 2-4 Hours after

E V Ivanov1, A B Berdalin2, Yu L Volkova2

  • 1Faculty of Fundamental Medicine, M. V. Lomonosov Moscow State University, Moscow, Russia. ivanovev101@gmail.com.

Bulletin of Experimental Biology and Medicine
|January 9, 2018
PubMed

Insights

This study shows that inducible nitric oxide synthase (iNOS) mRNA expression and neutrophil infiltration increase in rat hearts during ischemia and ischemia/reperfusion. These changes occur in both ischemic and non-ischemic tissues.

Area of Science:

  • Cardiovascular Science
  • Molecular Biology
  • Pathophysiology

Background:

  • Myocardial ischemia and reperfusion injury are significant clinical concerns.
  • The role of inducible nitric oxide synthase (iNOS) and neutrophil infiltration in these processes requires further elucidation.

Purpose of the Study:

  • To investigate the temporal expression of inducible NO-synthase (iNOS) mRNA.
  • To quantify myocardial infiltration with neutrophils.
  • To compare these responses in permanent ischemia and ischemia/reperfusion models in rats.

Main Methods:

  • Rats were subjected to permanent ischemia or ischemia/reperfusion models.
  • Expression of iNOS mRNA was analyzed using quantitative methods.
  • Myocardial neutrophil infiltration was assessed through histological examination.

Main Results:

  • iNOS mRNA expression significantly increased in the ischemic region in both models, with distinct temporal patterns.
  • Myocardial neutrophil infiltration was elevated compared to controls throughout the experiment.
  • Enhanced iNOS mRNA expression and neutrophil infiltration were also noted in non-ischemic myocardium.

Conclusions:

  • Both permanent ischemia and ischemia/reperfusion induce significant iNOS mRNA expression and neutrophil infiltration in the myocardium.
  • These inflammatory responses extend to non-ischemic areas, suggesting a broader impact of ischemic events.
  • Findings highlight the complex inflammatory cascade involved in myocardial injury.
Keywords:
inducible NO synthasemyocardial infiltrationmyocardial ischemianitric oxide

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