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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
