| Abstract: | BACKGROUND:Neonatal cerebral palsy is mainly caused by prenatal factors.At present,an animal model of prenatal infection and early postnatal hypoxia does not exist.OBJECTIVE:To observe morphology and motor performance following prenatal infection and hypoxic insult-induced brain damage of neonatal rats to verify the feasibility to establish a model of cerebral palsy.DESIGN,TIME AND SETTING:A randomized,controlled,animal experiment was performed at the Laboratories of Xinjiang Center for Disease Control and Prevention from September 2007 to June2008.MATERIALS:The hypoxic incubator was purchased from Shanghai Pediatric Medical Institute,China.Lipopolysaccharide(LPS,Escherichia coli,055:B5)was purchased from Sigma-Aldrich(St.Louis,MO,USA).METHODS:A total of 27 Wistar rats,aged 7 days,were randomly assigned to sham-surgery group(n = 15)with no carotid artery incision or hypoxia treatment,hypoxia/ischemia(H/I)group(n = 12)undergoing ligature of the right common carotid artery followed by exposure to hypoxia at postnatal day 7(P7),and LPS/H group(n = 19),in which pregnant rats were exposed in utero to LPS followed by prenatal hypoxia at embryonic day 16.MAIN OUTCOME MEASURES:Behavior,compound muscle action potential,and pathological changes were observed in 28-day-old rats.RESULTS:The footprint repeat space showed that left limb footprint repeatability in the H/I and LPS/H groups was lower than in the sham-surgery group(P< 0.05).The space between the footprints was larger and unstable.Hind limb quadricep compound muscle action potential in the H/I and LPS/H groups showed lower wave amplitude compared with the sham-surgery group(P< 0.05).Hematoxylin and eosin staining showed irregular cells around the ventricle,as well as periventricular leukomalacia.CONCLUSION:An animal model of cerebral palsy was established,which simulated the human condition most likely associated with occurrence of this disease.This model could be used for experimental studies related to cerebral patsy. |
