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
2010年
6期
329-330,333
,共3页
杨勐航%邵晓光%孙学军%郑娟
楊勐航%邵曉光%孫學軍%鄭娟
양맹항%소효광%손학군%정연
高压氧%惊厥%急性氧中毒%超氧化物歧化酶%一氧化氮
高壓氧%驚厥%急性氧中毒%超氧化物歧化酶%一氧化氮
고압양%량궐%급성양중독%초양화물기화매%일양화담
Hyperbaric oxygen%Convulsion%Acute oxygen toxicity%Superoxide dismutase%Nitric oxide
目的 研究高压氧预暴露对大鼠急性氧中毒潜伏期的影响并探讨其机制.方法 将40只Sprague-Dawley(SD)大鼠随机分为对照组和高压氧预暴露组,每组20只,其中高压氧预暴露组于高压纯氧(0.3 MPa)下暴露20 min,然后减至常压行空气通风20 min,如此循环4次.24 h后,将2组大鼠暴露于高压纯氧(0.5 MPa),观察40 min.检测指标包括惊厥潜伏期变化、大鼠脑组织中超氧化物歧化酶(SOD)活性和一氧化氮(NO)含量变化,进行HE染色以观察脑组织病理改变.结果 高压氧预暴露后,大鼠惊厥潜伏期[(29.79±2.13)min]比对照组[(24.25±3.76)min]延长,脑组织NO含量[(2.93±0.39)nmol/g]比对照组[(7.46±1.11)nmol/g]减少,而SOD活性与HE染色结果 显示2组差异无统计学意义.结论 高压氧预暴露可以延长大鼠惊厥潜伏期,其机制可能是高压氧降低了脑组织中的NO含量.
目的 研究高壓氧預暴露對大鼠急性氧中毒潛伏期的影響併探討其機製.方法 將40隻Sprague-Dawley(SD)大鼠隨機分為對照組和高壓氧預暴露組,每組20隻,其中高壓氧預暴露組于高壓純氧(0.3 MPa)下暴露20 min,然後減至常壓行空氣通風20 min,如此循環4次.24 h後,將2組大鼠暴露于高壓純氧(0.5 MPa),觀察40 min.檢測指標包括驚厥潛伏期變化、大鼠腦組織中超氧化物歧化酶(SOD)活性和一氧化氮(NO)含量變化,進行HE染色以觀察腦組織病理改變.結果 高壓氧預暴露後,大鼠驚厥潛伏期[(29.79±2.13)min]比對照組[(24.25±3.76)min]延長,腦組織NO含量[(2.93±0.39)nmol/g]比對照組[(7.46±1.11)nmol/g]減少,而SOD活性與HE染色結果 顯示2組差異無統計學意義.結論 高壓氧預暴露可以延長大鼠驚厥潛伏期,其機製可能是高壓氧降低瞭腦組織中的NO含量.
목적 연구고압양예폭로대대서급성양중독잠복기적영향병탐토기궤제.방법 장40지Sprague-Dawley(SD)대서수궤분위대조조화고압양예폭로조,매조20지,기중고압양예폭로조우고압순양(0.3 MPa)하폭로20 min,연후감지상압행공기통풍20 min,여차순배4차.24 h후,장2조대서폭로우고압순양(0.5 MPa),관찰40 min.검측지표포괄량궐잠복기변화、대서뇌조직중초양화물기화매(SOD)활성화일양화담(NO)함량변화,진행HE염색이관찰뇌조직병리개변.결과 고압양예폭로후,대서량궐잠복기[(29.79±2.13)min]비대조조[(24.25±3.76)min]연장,뇌조직NO함량[(2.93±0.39)nmol/g]비대조조[(7.46±1.11)nmol/g]감소,이SOD활성여HE염색결과 현시2조차이무통계학의의.결론 고압양예폭로가이연장대서량궐잠복기,기궤제가능시고압양강저료뇌조직중적NO함량.
Objective To investigate the effect of hyperbaric oxygen pretreatment on the latency of acute oxygen toxicity in rats and explore its mechanism. Methods Adult male SD rats were randomly divided into 2 groups: the control group and the hyperbaric oxygen pretreatment (HBOP) group. Rats in the HBOP group were exposed to pure hyperbaric oxygen for 20 min and then were decompressed to normal pressure and ventilated with air for another 20 min for a total of 4 sessions. Then, after 24 hours, the two animal groups were exposed to hyperbaric oxygen at a pressure of 0.5 MPa for 40 min. Measurement indices included changes in the latency of oxygen convulsion, activity of superoxide dismutase(SOD) and also contents of nitric oxide(NO)in the rat brain. The levels of NO and SOD in the brain tissue were also measured. HE staining was used to detect histological changes in the brain tissue. Results HBO pretreatment could significantly prolong the latency of oxygen convulsion, and also markedly reduce the content of nitric oxide(NO). SOD activity and HE staining indicated that no statistical differences could be seen in the 2 groups. Conclusions HBO pretreatment could prolong the latency of oxygen convulsion, the mechanism of which might suggest that HBO exposure could decrease the content of NO in the brain tissue.
