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[The relationship between the production of nitric oxide and the injury of cardiomyocytes caused by in vivo rat regional myocardial ischemia and reperfusion].

Authors
  • timoshin, A A
  • Tskitishvili, O V
  • Drobotova, D Iu
  • Studneva, I M
  • Serebriakova, L I
  • Ruuge, E K
  • Pisarenko, O I
Type
Published Article
Journal
Biofizika
Publication Date
Jan 01, 2008
Volume
53
Issue
4
Pages
679–683
Identifiers
PMID: 18819287
Source
Medline
License
Unknown

Abstract

Changes in nitric oxide concentration in rat myocardium in vivo during temporary occlusion of the anterior descending coronary artery, followed by reperfusion were studied by microdialysis assay in risk and intact areas by using an NO spin trap (complex of ferrous ions with N-methyl-D, L-glucamine dihiocarbamate, Fe3+-MGD2). The amplitude of the EPR signal of the NO spin adduct NO-Fe2+-MGD2 in the risk area increased during the 40-min occlusion and remained higher than the initial level during 60-min postischemic reperfusion, indicating a substantial nitric oxide production. The size of the infarction in the risk area by the end of reperfusion was 47 +/- 3 %, the contents of ATP, phosphocreatine, and total creatine decreased to 44 +/- 4, 51 +/- 5, and 60 +/- 3 %, correspondingly, as compared with initial values, and the level of lactate was six times higher than the initial one. In the intact area of the left ventricle, the level of nitric oxide and high-energy metabolites did not change throughout the experiment. It was shown that the intensive nitric oxide production, in acute regional ischemia and reperfusion are related to the disturbance of energy metabolism, the damage to cytoplasmic membranes, and the death of cardiomyocytes.

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