中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
2012年
5期
276-279
,共4页
方以群%刘景昌%刘长云%包晓辰%陈海庭
方以群%劉景昌%劉長雲%包曉辰%陳海庭
방이군%류경창%류장운%포효신%진해정
氧惊厥%一氧化氮合酶%一氧化氮%高压氧
氧驚厥%一氧化氮閤酶%一氧化氮%高壓氧
양량궐%일양화담합매%일양화담%고압양
Oxygen-induced convulsions%Nitric oxide synthase%Nitric oxide%Hyperbaric oxygen
目的 探讨一氧化氮合酶基因在氧惊厥发生机制中的作用.方法 40只SD大鼠按数字表法随机分为5组:正常对照组、氧惊厥组、惊厥前组、氮氧组、抑制剂+高压氧(HBO)组,每组8只.氧惊厥组:实验动物放入动物高压氧舱内,用纯氧加压至600 kPa,当动物发生惊厥大发作时减压.惊厥前组:纯氧加压至600 kPa,动物出现惊厥前期症状时开始减压.氮氧组:动物在含氧3.5%的氮氧混合气下,在600 kPa停留30 min,再减压.抑制剂+HBO组:动物进舱前10 min腹腔注射L-NAME(Nω-硝基-L-精氨酸甲酯),其他处理同氧惊厥组.正常对照组:动物置于加压舱内,模拟除压力和氧浓度以外的其他实验条件.各组动物出舱后取海马组织,抽提RNA后,逆转录聚合酶链反应(RT-PCR)测定各组iNOS、nNOS的mRNA表达量变化.结果 相对于正常对照组(0.3563±0.1036,0.5625±0.1035),氧惊厥组和抑制剂+HBO组海马组织中的iNOS(0.5513±0.1253,0.8588±0.1062)和nNOS(0.9300±0.1061,1.2238±0.1374)的表达均显著增加(P<0.05或P<0.01);氮氧组NOS基因表达改变不明显;NOS抑制剂可诱导氧惊厥动物海马组织的NOS基因表达.结论 NOS抑制剂可通过不完全阻断NOS的合成,延缓氧中毒的发作及降低发作程度,在氧惊厥发病机制中起重要作用.
目的 探討一氧化氮閤酶基因在氧驚厥髮生機製中的作用.方法 40隻SD大鼠按數字錶法隨機分為5組:正常對照組、氧驚厥組、驚厥前組、氮氧組、抑製劑+高壓氧(HBO)組,每組8隻.氧驚厥組:實驗動物放入動物高壓氧艙內,用純氧加壓至600 kPa,噹動物髮生驚厥大髮作時減壓.驚厥前組:純氧加壓至600 kPa,動物齣現驚厥前期癥狀時開始減壓.氮氧組:動物在含氧3.5%的氮氧混閤氣下,在600 kPa停留30 min,再減壓.抑製劑+HBO組:動物進艙前10 min腹腔註射L-NAME(Nω-硝基-L-精氨痠甲酯),其他處理同氧驚厥組.正常對照組:動物置于加壓艙內,模擬除壓力和氧濃度以外的其他實驗條件.各組動物齣艙後取海馬組織,抽提RNA後,逆轉錄聚閤酶鏈反應(RT-PCR)測定各組iNOS、nNOS的mRNA錶達量變化.結果 相對于正常對照組(0.3563±0.1036,0.5625±0.1035),氧驚厥組和抑製劑+HBO組海馬組織中的iNOS(0.5513±0.1253,0.8588±0.1062)和nNOS(0.9300±0.1061,1.2238±0.1374)的錶達均顯著增加(P<0.05或P<0.01);氮氧組NOS基因錶達改變不明顯;NOS抑製劑可誘導氧驚厥動物海馬組織的NOS基因錶達.結論 NOS抑製劑可通過不完全阻斷NOS的閤成,延緩氧中毒的髮作及降低髮作程度,在氧驚厥髮病機製中起重要作用.
목적 탐토일양화담합매기인재양량궐발생궤제중적작용.방법 40지SD대서안수자표법수궤분위5조:정상대조조、양량궐조、량궐전조、담양조、억제제+고압양(HBO)조,매조8지.양량궐조:실험동물방입동물고압양창내,용순양가압지600 kPa,당동물발생량궐대발작시감압.량궐전조:순양가압지600 kPa,동물출현량궐전기증상시개시감압.담양조:동물재함양3.5%적담양혼합기하,재600 kPa정류30 min,재감압.억제제+HBO조:동물진창전10 min복강주사L-NAME(Nω-초기-L-정안산갑지),기타처리동양량궐조.정상대조조:동물치우가압창내,모의제압력화양농도이외적기타실험조건.각조동물출창후취해마조직,추제RNA후,역전록취합매련반응(RT-PCR)측정각조iNOS、nNOS적mRNA표체량변화.결과 상대우정상대조조(0.3563±0.1036,0.5625±0.1035),양량궐조화억제제+HBO조해마조직중적iNOS(0.5513±0.1253,0.8588±0.1062)화nNOS(0.9300±0.1061,1.2238±0.1374)적표체균현저증가(P<0.05혹P<0.01);담양조NOS기인표체개변불명현;NOS억제제가유도양량궐동물해마조직적NOS기인표체.결론 NOS억제제가통과불완전조단NOS적합성,연완양중독적발작급강저발작정도,재양량궐발병궤제중기중요작용.
Objective To investigate the effect of nitric oxide synthase genes on the mechanism of oxygen-induced convulsions.Methods Forty healthy male Sprague-Dawley rats were chosen at random and divided into 5 groups:the normal control group,the model group(the oxygen-induced convulsions group),the convulsion group before decompression,the N2-O2 mixture group and the inhibitor+HBO group,each consisting of 8 animals.Rats in the model group were exposed to 600 kPa HBO and decompression was implemented,when convulsive seizures were present.Rats in the convulsion group before decompression were also exposed to 600 kPa HBO and decompression started,before precursor symptoms were present.Rats in the N2-O2 mixture group were exposed to 600 kPa N2-O2 mixture containing 3.5% oxygen for 30min,then they were decompressed.Rats in the inhibitor+HBO group were given an abdominal injection of Nω-nitro-larginine methylester(L-NAME)10 minutes before entrance into the chamber.Other treatments were the same as those of the convulsion group.Following decompression to normal pressure,hippocampi of rats were collected and total RNA were prepared by using Trizol Reagent.The expression levels of mRNA in iNOS、nNOS genes in various groups were detected with RT-PCR.Results The expression levels of iNOS and nNOS were all significantly higher tham those of the animals in the convulsion group,when they were compared with those of the normal control group.For the animals in the N2-O2 mixture group,no significant changes could be detected in the expression of NOS genes.NOS inhibitor(L-NAME)could induce the expression of NOS genes in rats with convulsive seizures.Conclusions NOS seemed to play an important role in the pathogenesis of oxygeninduced convulsion.NOS inhibitor could delay the onset of oxygen convulsion and decrease the severity of seizure through incomplete blocking of NOS synthesis.