title: Reduction of reperfusion-induced ventricular fibrillation and infarct size via heme oxygenase-1 overexpression in isolated mouse hearts.
abstract: 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 nontransgenic (NTg) groups were exposed to 20 min of global ischemia and 120 min of reperfusion. Epicardial ECG 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 TTC method were carried out. Results shown here provide additional support for cardioprotective effects of HO-1 as evidenced by the reduced infarct size. Moreover, overexpression of the HO-1 efficiently reduced the incidence of ischemia/reperfusion (I/R)-induced VF in HO-1 Tg mice.
authors: Department of Pharmacology, Health Science Center, Faculty of Pharmacy, University of Debrecen, Debrecen, Hungary.
authors: Istvan
authors: I
authors: Bak
authors: Attila
authors: A
authors: Czompa
authors: Bela
authors: B
authors: Juhasz
authors: Istvan
authors: I
authors: Lekli
authors: Arpad
authors: A
authors: Tosaki
mesh_terms: D000818:Animals; D015870:Gene Expression; D051547:Heme Oxygenase-1 / Q000235:genetics / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D008822:Mice, Transgenic; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000201:enzymology*; D009206:Myocardium / Q000201:enzymology* / Q000473:pathology; D051381:Rats; D014693:Ventricular Fibrillation / Q000201:enzymology* / Q000209:etiology
chemical_list: D008565:Membrane Proteins; D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse