PMID- 27097979
OWN - NLM
STAT- MEDLINE
DCOM- 20180416
LR  - 20181202
IS  - 1442-200X (Electronic)
IS  - 1328-8067 (Linking)
VI  - 58
IP  - 12
DP  - 2016 Dec
TI  - Tolerance to ischemia reperfusion injury in a congenital heart disease model.
PG  - 1266-1273
LID - 10.1111/ped.13022 [doi]
AB  - BACKGROUND: Open heart surgery-associated ischemia/reperfusion (I/R) injury 
      affects postoperative outcome, and a leading cause of this is lipid peroxidation. 
      Congenital heart disease (CHD) patients, however, are less sensitive to I/R 
      injury. Although little is known about the underlying molecular mechanisms, 
      CHD-associated hypoxia alters the polyunsaturated fatty acid (PUFA) composition 
      of membranes, which are the preferential targets for reactive oxygen species 
      (ROS) generated during I/R. Here, using an animal model, we investigated the 
      molecular mechanisms underlying I/R tolerance in CHD. METHODS: In order to 
      reproduce I/R injury in vitro, we used a working heart perfusion model, isolated 
      from juvenile control and CHD model rats (CHD rats), and examined the recovery of 
      cardiac function during a period of I/R. PUFA composition of the plasma membrane 
      was determined on gas chromatography/mass spectrometry. Oxidative stress-related 
      cellular responses were investigated on immunoblotting, using antibodies against 
      nuclear factor erythroid 2-related factor (Nrf-2), hemeoxygenase-1 (HO-1), and 
      4-hydroxy-2-hexanal (4-HHE)-modified protein. RESULTS: 
      Ischemia/reperfusion-induced cardiac dysfunction was markedly suppressed in CHD 
      rats, compared with the control rats. n-3/n-6 PUFA ratio was significantly 
      increased in both the pre- and post-I/R phase in CHD rats, but not in the 
      controls. Four-HHE-modified protein, Nrf-2, and HO-1 were significantly increased 
      in CHD rats as well, compared with the controls. CONCLUSIONS: Following open 
      heart surgery in CHD patients, the increased n-3/n-6 PUFA ratio may lead to the 
      upregulation of cellular antioxidative system components through the oxidation 
      product, 4-HHE, resulting in an increased tolerance to I/R injury.
CI  - (c) 2016 Japan Pediatric Society.
FAU - Asada, Dai
AU  - Asada D
AD  - Department of Pediatric Cardiology and Nephrology, Graduate School of Medical 
      Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
FAU - Itoi, Toshiyuki
AU  - Itoi T
AD  - Department of Pediatric Cardiology and Nephrology, Graduate School of Medical 
      Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
FAU - Nakamura, Akihiro
AU  - Nakamura A
AD  - Department of Pediatric Cardiology and Nephrology, Graduate School of Medical 
      Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
FAU - Hamaoka, Kenji
AU  - Hamaoka K
AD  - Department of Pediatric Cardiology and Nephrology, Graduate School of Medical 
      Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
LA  - eng
PT  - Journal Article
DEP - 20160720
PL  - Australia
TA  - Pediatr Int
JT  - Pediatrics international : official journal of the Japan Pediatric Society
JID - 100886002
RN  - 0 (Reactive Oxygen Species)
SB  - IM
MH  - Animals
MH  - Disease Models, Animal
MH  - Heart Diseases/*congenital
MH  - Humans
MH  - Lipid Peroxidation
MH  - Oxidative Stress
MH  - Rats
MH  - Reactive Oxygen Species
MH  - *Reperfusion Injury
OTO - NOTNLM
OT  - antioxidant
OT  - congenital heart disease
OT  - ischemia/reperfusion injury
OT  - lipid peroxidation
OT  - polyunsaturated fatty acid
EDAT- 2016/04/22 06:00
MHDA- 2018/04/17 06:00
CRDT- 2016/04/22 06:00
PHST- 2016/01/22 00:00 [received]
PHST- 2016/03/16 00:00 [revised]
PHST- 2016/04/12 00:00 [accepted]
PHST- 2016/04/22 06:00 [pubmed]
PHST- 2018/04/17 06:00 [medline]
PHST- 2016/04/22 06:00 [entrez]
AID - 10.1111/ped.13022 [doi]
PST - ppublish
SO  - Pediatr Int. 2016 Dec;58(12):1266-1273. doi: 10.1111/ped.13022. Epub 2016 Jul 20.