Open AccessReduction of reperfusion‐induced ventricular fibrillation and infarct size via heme oxygenase‐1 overexpression in isolated mouse hearts
Author(s) -
Bak Istvan,
Czompa Attila,
Juhasz Bela,
Lekli Istvan,
Tosaki Arpad
Publication year - 2010
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2010.01142.x
Subject(s) - heme oxygenase , heme , ventricular fibrillation , cardiology , reduction (mathematics) , medicine , chemistry , enzyme , biochemistry , geometry , mathematics
Heme oxygenase‐1 (HO‐1), also known as heat shock protein 32 (hsp‐32) is a stress‐induced cytoprotective protein. The present investigation evaluated the capacity of HO‐1 to reduce the incidence of reperfusion‐induced ventricular fibrillation (VF) and infarct size. HO‐1 transgenic (Tg) mice were generated using a rat HO‐1 genomic transgene. Isolated mouse hearts obtained from Tg and non‐transgenic (NTg) groups were exposed to 20 min. of global ischemia and 120 min. of reperfusion. Epicardial electrocardiogram was recorded to monitor the incidence of reperfusion‐induced VF and at the end of the reperfusion period, detection of HO‐1 by immunohistochemistry and measurement of infarct size using the tetrazolium chloride method were carried out. Results shown here provide additional support for cardioprotective effects of HO‐1 as demonstrated by the reduced infarct size. Moreover, overexpression of the HO‐1 efficiently reduced the incidence of ischemia/reperfusion induced VF in HO‐1 Tg mice.