Augmentation of tissue nitric oxide and nitric oxide synthase (NOS) in myocardial ischemia-reperfusion (I-R)

Peitan Liu, Carl E. Hock, Patrick Y.K. Wona

Research output: Contribution to journalArticlepeer-review

Abstract

Myocardial I-R is associated with inflammation, arrhythmias and cardiac dysfunction. We have investigated the contribution of nitric oxide, the induction of iNOS and Superoxide to the inflammatory response induced by coronary artery ligation (20 min) and reperfusion (5 h). Male Sprague-Dawley rats were anesthetized and the left main coronary artery was ligated and reperfused. Myocardial I-R injury was confirmed using triphenyl tetrazolium chloride (TTC) staining. Superoxide and tissue nitrite/nitrate levels in the I-R region of the heart were increased by 235% and 205%, respectively, (p<0.02) compared to sham-operated controls. Superoxide and nitrite/nitrate values in the non-ischemic region were similar to those in the sham control group. Total NOS activity was elevated by 320% (p<0.05), however, inducible NOS (iNOS) activity was increased by 7.9-fold (p<0.001) in the ischémie vs non-ischemic regions; similar elevations were observed when compared to sham-operated control rats. iNOS accounted for 76% of the total NOS activity in the I-R region. Myocardial I-R induced both systemic and remote organ (lung) inflammatory responses. Circulating neutrophils were increased by 248% (p<0.001) and plasma nitrite/nitrate was increased by 231% (p< 0.001) in I-R rats compared to sham controls. Lung Superoxide generation was increased by 257% and lung nitrite/nitrate was increased by 151% (p<0.001) compared with sham control. Myocardial I-R resulted in significant elevations in nitrite/nitrate, Superoxide, total NOS and iNOS in the I-R region of the heart. Furthermore, the inflammatory response induced by myocardiai I-R was evident in both the ischémie region of the heart and in a remote organ (lung).

Original languageEnglish (US)
Pages (from-to)A13
JournalFASEB Journal
Volume10
Issue number3
StatePublished - 1996
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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