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Heme oxygenase‐1 related carbon monoxide production and ventricular fibrillation in isolated ischemic/reperfused mouse myocardium
Author(s) -
Bak Istvan,
Szendrei Levente,
Turoczi Tibor,
Papp Gabor,
Joo Ferenc,
Das Dipak K.,
Leiris Joel,
Der Peter,
Juhasz Bela,
Varga Edit,
Bacskay Ildiko,
Balla Jozsef,
Kovacs Peter,
Tosaki Arpad
Publication year - 2003
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.03-0032fje
Subject(s) - heme oxygenase , enzyme , endogeny , medicine , messenger rna , heme , enzyme assay , chemistry , endocrinology , biology , biochemistry , gene
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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