Objective To evaluate the role of prenatal chronic hypoxia on myocardial ischaemia /reperfusion injury in adult rabbits’ offspring and explore the relevant mechanism.
Methods The pregnant New Zealand rabbits were divided randomly into normoxic (n=8) and hypoxic (12% O2 from days 10 to 28 of gestation, n=8) groups. One male offspring of each maternal rabbit was randomly selected to study. The offspring rabbits were subjected to heat stress (42°C for 15 min) at 6 months of age. After 24 h, left anterior descending branches were excised and subjected to ischaemia for 30 min and reperfusion for 120 min. Cardiac histopathological observation was performed by light microscope and electron microscope. The expression of heat shock protein 70 (HSP70) in myocardium was detected by immunohistochemistry. Myocardial enzyme activity, apoptotic index and caspase−3 activity in myocardium were examined as well.
Results Ischemia-reperfusion after heat stress pretreatment increased myocardial enzyme activity, apoptotic index and caspase−3 activity in prenatal chronic hypoxia rabbits (4720.31±744.39 IU/l, 1849.13±416.58 IU/l, 40.43±5.03%, 12.43±1.77 unit, respectively) when compared with control (3388.95±532.43 IU/l, 1435.13±92.08 IU/l, 34.40±4.66%, 10.58±1.42 unit, respectively). Heat stress pretreatment induced HSP70 significant expression in left ventricular myocardium was not observed in prenatal chronic hypoxia rabbits but in normoxic control rabbits.
Conclusions Prenatal chronic hypoxia inhibits HSP70 synthesis in the heart of adult offspring in response to body heat stress, which might insult cardioprotection against ischaemia-reperfusion injury.