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Paper Information

Title: 

EARLY PHASE OF HYPEROXIA ATTENUATES ISCHEMIA-REPERFUSION INDUCED APOPTOSIS IN HEART

Type: SPEECH
Author(s): FOUAD ALDINI M.*,ESMAEILI DEHAJ MANSOUR,MEHRANI H.,NOUROUZZADEH ALI,SAFARI FATEMEH,SHEKARFOROUSH SHAHNAZ,GOLMANESH L.,KHOUSHBATEN A.
 
 *DEPARTMENT OF PHYSIOLOGY AND PHARMACOLOGY, BIRJAND UNIVERSITY OF MEDICAL SCIENCES, BRIGAND, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

Pre-exposure to normobaric hyperoxia (NBO2) gas has been shown to protect the heart from ischemia-reperfusion injury. In the present study we investigated the effect of early phase of normobaric hyperoxia cardioprotection on myocardial necrosis and apoptosis. Rats were divided into two groups: control group were kept in normal air environment for 120 min, and then studied as In vivo heart model subjected to 30 min of local ischemia followed by 360 min of reperfusion, and hyperoxic group were kept in a hyperoxic (95%O2) environment for 120 min, immediately before subjected the ischemic-reperfusion protocol. Cardiac function was assessed by comparing hemodynamic and ischemic arrhythmia and myocardial injury by measurement of triphenyltetrazolium chloride (TTC) staining, terminal deoxy-nucleotidyl transferasemediated dUTP nick end-labeling (TUNEL), caspase 3 activity and bcl2 and bax proteins expression. Compared with control group, NBO2 could ameliorate ischemic arrhythmias, decrease infarct size (from 53.1±2.8 % to 26.9±2.2%, p<0.001), decrease bcl2 to bax ratio (from 44% to 24%, p<0.05), decrease caspase 3 activity (from 2.95±0.18% to 1.98±0.17%, p<0.05), and decrease TUNEL-positive (from 32.2±1.88% to 22.6±2.33%, p<0.05). In conclusion, hyperoxia can protect the rat heart against ischemic-reperfusion injury probably by decreasing of myocardial apoptosis

 
Keyword(s): NORMOBARIC HYPEROXIA, APOPTOSIS, NECROSIS, REPERFUSION
 
 
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