Changes Of SOD And MDA In Hypoxic-ischaemic Encephalopathy During And After Selective Head Cooling With Hypothermia

Objective:Neonatal hypoxic ischemic encephalopathy (hypoxic ischemic en-cephalopathy,H IE) is the result of perinatal diseases caused by severe neonatal hypoxic-ischemic brain damage,is the important reason of neonatal death and disability . At present ,HIE lack of effective treatment. The complexity of its pathogenesis has not yet been fully elucidated, pathological processes, including primary injury and reperfusion injury. Oxidative stress is a cerebral ischemia / reperfusion injury of the main factors. Free radical chain reactions is cerebral hypoxia ischemia pathological aspects of the core.Superoxide dismutase (SOD) as scavenger of oxygen free radicals, MDA (MDA) is the end product of lipid peroxidation, and hypoxia, ischemia- reperfusion and other acute injury are closely related. Therefore, the determination of the blood in children with HIE malondialdehyde (MDA) and superoxide dismutase (SOD) in serum of early diagnosis and determine the severity of HIE and treatment evaluation of important indicators..Therapeutic hypothermia is induced hypothermia lowers the core temperature of the brain by 2°C to 6°C for treatment. Recent a number of animal studies show that hypothermia is effective on neonatal animal brain.In terms of mechanisms of protective effect of hypothermia,studies have proposed that hypothermia might reduce energy consumption and anaerobic metabolism of cerebrum, reduce over- releasing and over- activation of extracellular excitotoxic amino acids, inhibit excessive accumulation of intracellular calcium,reduce production oxygen radical and NO,interfere inflammatory responses, attenuate cerebral edema and inhibit apoptosis.This experment by measuring before and after treatment the concentration of these two indicators to dynamic change, and further understanding of mild hypothermia on oxidative stress injury in HIE and neuroprotective mechanisms. For the clinical treatment of hypoxic ischemic encephalopathy provide a theoretical basis.Methods:1 Experiment objectsThe newborns of the intensive care unit in Hebei Province children hospital were selected, who entered newborn department on January, to December 2010, the embryo age exceed 37 weeks, the body weight exceed 2.5kilograms. HIE conformed to HIE diagnostic criteria in Diagnostic criteria for neonatal hypoxic-ischem ic encephalopathy in November 2004 by The Subspecialty Group of Neonatology, Pediatric Society, Chinese Medical Association.All infants were supplied with airtube intubation, irrigation of trachea,application with conventional therapy(sustain normal blood pressure and blood gas, sustain acid-base balance, confine fluid, control seizures, depress intracranial pressure and provid nutritional support, provid assisted respiration pro re nata).10 healthy full-term newborns borned in the same hospital in the same time were taken to the comparison group.2 The experiment groupsThe HIE infants were divided into the hypothermia group (Group A), and the conventional treatment comparison group (Group B), according to the random digits table, every group were divided into the moderate and severe, Group C for normal group.2.1 Group A of 28 examples, the average birth age 7.65±4.8h hours,the embryo age 39.3±1.07weeks, the birth body weight3.55±0.31kg (30 examples were selected, to give up the treatment 1 example, to be rejected because of sample haemolysis.);2.2 Group B 0f26 examples, the average birth age 7.86±5.4h hours,the embryo age 38.8±1.26 weeks, the birth body weight 3.63±0.29kg (30 examples were selected, to give up the treatment 2 example, to be rejected because of sample haemolysis.);2.3 Group C of 10 examples, the average birth age 7.46±4.4 hours,the embryo age38.9±1.49 weeks, the birth body weight 3.50±0.33 kg, were selected randomly on the same time of the same hospital, who born in 24hours, and were born in full-term, excepted for infection duration of pregnancy, congenital deformity, congenital metabolism dysfunction, intrauterine infection ,infection before or during delivery, severe intracranial hemorrhage, fracture of skull.3 Laboratory procedure3.1 Group A and Group B infants of selected accepted the conventional therapy, included providing adequate oxygen and glycose, sustaining normal blood pressure and blood gas, sustaining acid-base balance, confining fluid, controlling seizures, depressing intracranial pressure and providing nutritional support, providing assisted respiration pro re nata. Group A simultaneously accepted the Selective head cooling with hypothermia treatment. The entire journey two groups of infants were observed vital sign in whole range. The body temperature, the breath, the blood pressure,the blood routine,the clotting mechanism, seizures,w whether or not scleredema ere observed too.3.2 Group A were taken the venous blood 2ml when the hypothermia treatment (0h) and 24 hours (24h), 48hours (48h) 72 hours (72h),7days(7d) after therapy. With the 3500r/min centrifugalization 10 minutes, blood serum were accepted and set spare to -70℃refrigerator preservation. Group B were taken the venous blood 2ml when the hospitalization (0h) and 24 hours (24h) , 48hours (48h) ,72 hours (72h) , 7days(7d) after therapy. With the 3500r/min centrifugalization 10 minutes, blood serum were accepted and set spare to -70℃refrigerator preservation. Group C were taken 2ml venous blood when born (0h) and 24hours (24h) , 48hours (48h),72 hours (72h) , 7days(7d) after born and separated blood serum too. The blood serum were put into -70℃refrigerator for preservation.3.3 Serum levels of SOD and MDA using Determination of xanthine oxidase and hiobarbituric assay respectly before treatment and 24hrs,48hrs,72hrs and 7days after treatment . the examination step and the method carried on according to which the medicine kit showed. 4 The statistical analysis SPSS13.0 statistics software was used to carry on statistics processing, P<0.05(double side) had statistical significance.Results:1 There were no significance difference of SOD and MDA on 0h, 24h, 48 h 72h,7d with Group C.(P>0.05).2 Compared with GroupC, blood serum SODand MDA advanced in blood serum of Group B moderate and severe on 0h, 24h, 48h 72h,7d,there were significance differences in statistic(P<0.05).3 Compared with Group B moderate,SOD and MDA in blood serum in Group A moderate were significance differences in statistic (P<0.05) on 24hour,48hour 72hour and 7day after treatment. Compared with Group B severe, SOD and MDA in Group A severe of blood serum were significance differences in statistic (P<0.05).Conclusions:1 Hypoxic-ischemic oxygen free radicals produced after reperfusion increased SOD scavenging oxygen free radicals are a lot of consumption, increased lipid peroxidation, lipid peroxidation increased MDA formation, resulting in damage to nerve tissue, and further deterioration of promoting HIE .2 Treatment of hypothermia is hypoxic-ischemic brain injury in a new therapy can reduce brain tissue oxygen consumption, inhibition of endogenous toxic products of brain cell damage, reducing calcium influx, inhibition of apoptosis, decreased free base, inhibit the consumption of free radical scavengers and lipid oxidation chain, reducing protein damage brain cells and promote functional recovery of brain structure and to protect the blood-brain barrier, cerebral edema, low perfusion improved after ischemia and reperfusion injury.3 The experiment showed that mild hypothermia can inhibit selective oxygen free radicals, oxygen free generation and a chain reaction was inhibited, reducing the consumption of SOD, Paul oxidase, antioxidant protection of brain tissue, and can stabilize the plasma membrane of cell so as to reduce lipid peroxidation and reduce the formation of its metabolite MDA, reduce lipid peroxidation of brain tissue damage, thus reducing the ischemic nerve cell membrane and organelle damage, thereby protecting brain tissue.