地塞米松在新生猪缺氧缺血性脑损伤中的防治作用

A STUDY ON EFFECT OF DEXAMETHASONEON THE HYPOXIC-ISCHEMIC BRAIN DAM-AGE OF NEWBORN PIG

采用结扎新生猪一侧颈总动脉，并将其置于含８％氧气和９２％氮气的环境中，做成缺氧缺血性脑病（ＨＩＥ）的动物模型。检查ＨＩＥ模型组、正常对照组、大剂量地塞米松（１０ｍｇ／ｋｇ）治疗组和小剂量地塞米松（０．５ｍｇ／ｋｇ）治＋疗组（共３７只）脑组织脂质过氧化物（ＬＰＯ）、超氧化物歧化酶（ＳＯＤ）含量及病理改变。结果表明：ＨＩＥ模型组ＬＰＯ较正常组增高，ＳＯＤ降低，大剂量地塞米松治疗组ＬＰＯ、ＳＯＤ含量及病理改变均较模型组有明显改善，而小剂量地塞米松治疗组则无明显改善。提示自由基参与了缺氧缺血性脑损伤，而地塞米松可能具有保扩作用。

AbstractThe animal model of hypoxic-ischemiceneephalopathy (HIE) was set up by ligating unilateralcarotid artery of the newborn pigs and exposing themto 8% oxygen. The lipid peroxidation (LPO) andsuperoxide dismutase (SOD) of the brain tissue andbrain pathology were investigated in all 37 newbornpigs which were divided into four groups: nonnal con-trol (n=7), HIE model group (n=11), high-dosedexamethasone (10mg / kg) treatment group (n = 10),and low-dose dexamethasone (0.5mg / kg) treatmentgroup (n=9). The results showed that LPO of braintissue was significantly elevated and SOD wassignificantly decreased in HIE model group, and LPO,SOD contents and pathologic changes were allsignificantly improved in highAsose dexamethasonetreatment group. There was no significant differenceand improvement in LPO, SOD contents and patholo-gy between HIE model and lowdose dexamethasonetreatment groups. This study suggests that free radiclesplay a role in pathogenesis of HIE and dexamethasonepossibly has eertain protective effect in HIE.