亚低温对新生鼠缺氧缺血性脑损伤自由基影响的研究

The Effect of Mild Hypothermia on Free Radicals in the Hypoxic-Ischemic Brain Damage of Neonatal Rat

目的 研究亚低温对新生鼠缺氧缺血性脑损伤后自由基的影响。 方法 7日龄大鼠行左侧颈总动脉结扎后吸入8%氧气 2h ,制成缺氧缺血性脑损伤模型。动物随机分成五组 :假手术组、缺氧缺血组、缺氧缺血后 30min给予亚低温组、缺氧缺血后 1h给予亚低温组、缺氧缺血后 3h给予亚低温组。脑皮质细胞匀浆用于测定丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)活性。 结果 缺氧缺血组MDA含量明显高于假手术组 ,而亚低温各组MDA含量均低于缺氧缺血组 ,而且亚低温应用越早者MDA含量减少越明显。 结论

Objective The aim of this study is to determine the effect of mild hypothermia on free radicals in the neonate hypoxic-ischemic brain damage(HIBD).Methods The HIBD model was produced in the traditional model of neonatal hypoxic-ischemic(HI)which subjected 7-old-day Wistar rats to unilateral carotid artery ligation followed by an hypoxia(8% oxyger)episode of 2 hours duration.The rats were divided into five groups randomly.Group Ⅰ:sham-operated.Group Ⅱ:No treatment was applied to animal after hypoxia-ischemia onset.Group Ⅲ:4 hours of hypothemia was applied to animal at 30 minutes after the hypoxia-ischemia onset.Group Ⅳ:Hypothermia was applied at 1 hours after hypoxia-ishemia onset.Group Ⅴ:Hypothermia was applied at 3 hours after the hypoxia-ischemia onset.The homogenate of cortical cells was used to determine malonyldialdehyde(MDA)content and superoxide dismutase(SOD)activities.Results The MDA content of group Ⅱ was significantly higher than group I( P<0 01); the MDA content of groups subjected to hypothermia were all lower than group Ⅱ,and the earlier the use of hypothermia,the lower the content of MDA.Conclusion These results demonstrated that hypothermia can prevent hyposic-ishemic brain damage by suppressing the generation of free radicals. Key words:cerebral hypoxic ischemia;hypothermia;free radicaltion of arrhythmogenic right ventricular cardiomyopathy$$$$ Yang Lixian. Huizhou People's Hospital, Huizhou 516002 Abstract Objective By analysing cases of ARVC we encountered and reviewed related literaturts, to deepen the understanding of ARVC, especially early recoganizing arrhythmia with unknown aetiology in young and middleaged and prevention of sudden death. Discussion At present, ARVC is generally believed a autosomal hereditary disease and may be dominance, partial dominance or larval. It is also suggested that cardiac muscle replaced by fatty tissue is the result of acquired injury (inflammation, necrosis) caused by chronic myocarditis and repairing process.Diagnosis Diagnosis is mainly based upon clinical symptoms such as palpilation, dizziness, syncope, combined with typical electrocardiogram of ventricular premature beats, paroxysmal tachyarrhythmia, ventricular fibrillation, QRS time limit ≥110ms, Furthmore, evaluation of the shape and function of the heart should be performed. Histological examination is the gold standard for diagnosis of ARVC, but must pay attention to the site of drawing material during endocardial biopsy to avoid ventricular wall perforation. Treatment ARVC is usually treated with antiarrhythmic drug. severe cases could be treated by implanting defibrillator or undergoing heart transplantation.