Reduction of reperfusion-induced ventricular fibrillation and infarct size via heme oxygenase-1 overexpression in isolated mouse hearts

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.