INVOLVEMENT OF NO-SYNTHASE IN THE INFARCT REDUCING EFFECT OF CONTINUOUS CHRONIC NORMOBARTC HYPOXTA

N. V. Naryzhnaya, L. N. Maslov, S. Yu Tsibulnikov, E. S. Prokudina, Yu B. Lishmanov

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Abstract

It was investigated the role of inducible and endothelial NO-synthase (NOS) in the infaret reducing effect of chronic continuous normobaric hypoxia (CCNH) on the model of coronary artery occlusion and reperfusion in rats. Rats were subjected to hypoxic exposure (12% O2 during 21 days). It has found that CCNH causes an increase in total levels of nitrate and nitrite in deproteinized blood serum in 1.5-fold and 2-fold in myocardium compared with intact animals. This effect is manifested in intact animals and in rats with a 20 minute coronary artery occlusion and reperfusi- on. Chronic continuous normobaric hvoxia exhibited infarct soaring effect. which does not manifest after pretreatment with NO-synthase inhibitor NAME (10 mg/kg intravenously), the selective inhibitor of inducible NOS S-methylisothiourea (3 mg/kg intraperitoneally), but remained after blocking neuronal NOS with 7-nitronidazol (50 mg/kg intravenously). The findings suggest that the inducible NO-synthase and nitric oxide play an important role in the implementation of the infaret limiting effect of chronic continuous normobaric hvnoxia.

Original languageEnglish
Pages (from-to)921-928
Number of pages8
JournalRossiǐskii fiziologicheskiǐ zhurnal imeni I.M. Sechenova / Rossiǐskaia akademiia nauk
Volume101
Issue number8
Publication statusPublished - 1 Aug 2015

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Nitric Oxide Synthase
Myocardial Reperfusion
Coronary Occlusion
Coronary Vessels
Nitric Oxide Synthase Type II
Nitrites
Nitrates
Myocardium
Serum
Hypoxia

ASJC Scopus subject areas

  • Medicine(all)

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INVOLVEMENT OF NO-SYNTHASE IN THE INFARCT REDUCING EFFECT OF CONTINUOUS CHRONIC NORMOBARTC HYPOXTA. / Naryzhnaya, N. V.; Maslov, L. N.; Tsibulnikov, S. Yu; Prokudina, E. S.; Lishmanov, Yu B.

In: Rossiǐskii fiziologicheskiǐ zhurnal imeni I.M. Sechenova / Rossiǐskaia akademiia nauk, Vol. 101, No. 8, 01.08.2015, p. 921-928.

Research output: Contribution to journalArticle

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