Heme oxygenase-1-related carbon monoxide production and ventricular fibrillation in isolated ischemic/reperfused mouse myocardium.

I. Bak, Levente Szendrei, Tibor Turoczi, Gabor Papp, Ferenc Joo, Dipak K. Das, Joel de Leiris, Peter Der, B. Juhász, E. Varga, I. Bácskay, J. Balla, Peter Kovacs, A. Tósaki

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Abstract

Heme oxygenase-1 (HO-1)-dependent carbon monoxide (CO) production related to reperfusion-induced ventricular fibrillation (VF) was studied in HO-1 wild-type (+/+), heterozygous (+/-), and homozygous (-/-) isolated ischemic/reperfused mouse heart. In HO-1 homozygous myocardium, under aerobic conditions, HO-1 enzyme activity, HO-1 mRNA, and protein expression were not detected in comparison with aerobically perfused wild-type and heterozygous myocardium. In wild-type, HO-1 hetero- and homozygous hearts subjected to 20 min ischemia followed by 2 h of reperfusion, the expression of HO-1 mRNA, protein, and HO-1 enzyme activity was detected in various degrees. A reduction in the expression of HO-1 mRNA, protein, and enzyme activity in fibrillated wild-type and heterozygous myocardium was observed. In reperfused/nonfibrillated wild-type and heterozygous hearts, a reduction in HO-1 mRNA, protein expression, and HO-1 enzyme activity was not observed, indicating that changes in HO-1 mRNA, protein, and enzyme activity could be related to the development of VF. These changes were reflected in the HO-1-related endogenous CO production measured by gas chromatography. In HO-1 knockout ischemic/reperfused myocardium, all hearts showed VF, and no detection in HO-1 mRNA, protein, and enzyme activity was observed. Thus, interventions that are able to increase endogenous CO may prevent the development of VF.

Original languageEnglish
Pages (from-to)2133-2135
Number of pages3
JournalFASEB Journal
Volume17
Issue number14
Publication statusPublished - 2003

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Heme Oxygenase-1
Ventricular Fibrillation
Carbon Monoxide
Myocardium
Enzyme activity
Messenger RNA
Enzymes
Proteins
Reperfusion
Gas chromatography
Gas Chromatography

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Heme oxygenase-1-related carbon monoxide production and ventricular fibrillation in isolated ischemic/reperfused mouse myocardium. / Bak, I.; Szendrei, Levente; Turoczi, Tibor; Papp, Gabor; Joo, Ferenc; Das, Dipak K.; de Leiris, Joel; Der, Peter; Juhász, B.; Varga, E.; Bácskay, I.; Balla, J.; Kovacs, Peter; Tósaki, A.

In: FASEB Journal, Vol. 17, No. 14, 2003, p. 2133-2135.

Research output: Contribution to journalArticle

Bak, I. ; Szendrei, Levente ; Turoczi, Tibor ; Papp, Gabor ; Joo, Ferenc ; Das, Dipak K. ; de Leiris, Joel ; Der, Peter ; Juhász, B. ; Varga, E. ; Bácskay, I. ; Balla, J. ; Kovacs, Peter ; Tósaki, A. / Heme oxygenase-1-related carbon monoxide production and ventricular fibrillation in isolated ischemic/reperfused mouse myocardium. In: FASEB Journal. 2003 ; Vol. 17, No. 14. pp. 2133-2135.
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abstract = "Heme oxygenase-1 (HO-1)-dependent carbon monoxide (CO) production related to reperfusion-induced ventricular fibrillation (VF) was studied in HO-1 wild-type (+/+), heterozygous (+/-), and homozygous (-/-) isolated ischemic/reperfused mouse heart. In HO-1 homozygous myocardium, under aerobic conditions, HO-1 enzyme activity, HO-1 mRNA, and protein expression were not detected in comparison with aerobically perfused wild-type and heterozygous myocardium. In wild-type, HO-1 hetero- and homozygous hearts subjected to 20 min ischemia followed by 2 h of reperfusion, the expression of HO-1 mRNA, protein, and HO-1 enzyme activity was detected in various degrees. A reduction in the expression of HO-1 mRNA, protein, and enzyme activity in fibrillated wild-type and heterozygous myocardium was observed. In reperfused/nonfibrillated wild-type and heterozygous hearts, a reduction in HO-1 mRNA, protein expression, and HO-1 enzyme activity was not observed, indicating that changes in HO-1 mRNA, protein, and enzyme activity could be related to the development of VF. These changes were reflected in the HO-1-related endogenous CO production measured by gas chromatography. In HO-1 knockout ischemic/reperfused myocardium, all hearts showed VF, and no detection in HO-1 mRNA, protein, and enzyme activity was observed. Thus, interventions that are able to increase endogenous CO may prevent the development of VF.",
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