In:
Pediatrics International, Wiley, Vol. 58, No. 12 ( 2016-12), p. 1266-1273
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
1328-8067
,
1442-200X
DOI:
10.1111/ped.2016.58.issue-12
Language:
English
Publisher:
Wiley
Publication Date:
2016
detail.hit.zdb_id:
2008621-0
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