中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2008年
12期
707-709,前插7
,共4页
吗啡,肿瘤坏死因子-α%心肌缺血,急性%肺
嗎啡,腫瘤壞死因子-α%心肌缺血,急性%肺
마배,종류배사인자-α%심기결혈,급성%폐
morphine%tumor necrosis factor-α%acute myocardial ischemia%lung
目的 观察急性心肌缺血大鼠肺组织中肿瘤坏死因子-α(TNF-α)的表达变化以及吗啡硬膜外给药的干预效应.方法 将健康成年雄性SD大鼠18只随机分为假手术组(S组)、结扎冠状动脉(冠脉)缺血组(CAO组)和吗啡预处理组(M组),每组6只.S组动物仅开胸,不结扎左冠脉前降支;CAO组动物开胸后结扎左冠脉前降支;M组动物在结扎左冠脉前降支前15 min经硬膜外注射吗啡60μg/kg.各组在开胸或扎闭左冠脉前降支后3 h开胸取右肺下叶,采用免疫组化、酶联免疫吸附法(ELISA)检测肺组织中TNF-α表达变化.结果 免疫组化结果显示,与S组比较(8.68±0.29,1.609±0.050),CAO组(24.55±6.25,1.844±0.027)和M组(11.60±1.21,1.733±0.027)气管TNF-α阳性单位及平均吸光度(A)值均明显升高,而M组较CAO组明显降低,差异均有统计学意义(P均<0.01).ELISA结果显示:CAO组[(221.58±5.23)ng/L]和M组[(103.45±4.56)ng/L3肺组织TNF-α阳性免疫反应物质的表达水平均高于S组E(47.14±1.36)ng/L),且M组显著低于CAO组(P均<0.01).结论 急性心肌缺血能通过神经机制介导肺脏TNF-α表达上调;阿片类物质及其受体机制参与了机体内心脏伤害性神经信号转导的调节.
目的 觀察急性心肌缺血大鼠肺組織中腫瘤壞死因子-α(TNF-α)的錶達變化以及嗎啡硬膜外給藥的榦預效應.方法 將健康成年雄性SD大鼠18隻隨機分為假手術組(S組)、結扎冠狀動脈(冠脈)缺血組(CAO組)和嗎啡預處理組(M組),每組6隻.S組動物僅開胸,不結扎左冠脈前降支;CAO組動物開胸後結扎左冠脈前降支;M組動物在結扎左冠脈前降支前15 min經硬膜外註射嗎啡60μg/kg.各組在開胸或扎閉左冠脈前降支後3 h開胸取右肺下葉,採用免疫組化、酶聯免疫吸附法(ELISA)檢測肺組織中TNF-α錶達變化.結果 免疫組化結果顯示,與S組比較(8.68±0.29,1.609±0.050),CAO組(24.55±6.25,1.844±0.027)和M組(11.60±1.21,1.733±0.027)氣管TNF-α暘性單位及平均吸光度(A)值均明顯升高,而M組較CAO組明顯降低,差異均有統計學意義(P均<0.01).ELISA結果顯示:CAO組[(221.58±5.23)ng/L]和M組[(103.45±4.56)ng/L3肺組織TNF-α暘性免疫反應物質的錶達水平均高于S組E(47.14±1.36)ng/L),且M組顯著低于CAO組(P均<0.01).結論 急性心肌缺血能通過神經機製介導肺髒TNF-α錶達上調;阿片類物質及其受體機製參與瞭機體內心髒傷害性神經信號轉導的調節.
목적 관찰급성심기결혈대서폐조직중종류배사인자-α(TNF-α)적표체변화이급마배경막외급약적간예효응.방법 장건강성년웅성SD대서18지수궤분위가수술조(S조)、결찰관상동맥(관맥)결혈조(CAO조)화마배예처리조(M조),매조6지.S조동물부개흉,불결찰좌관맥전강지;CAO조동물개흉후결찰좌관맥전강지;M조동물재결찰좌관맥전강지전15 min경경막외주사마배60μg/kg.각조재개흉혹찰폐좌관맥전강지후3 h개흉취우폐하협,채용면역조화、매련면역흡부법(ELISA)검측폐조직중TNF-α표체변화.결과 면역조화결과현시,여S조비교(8.68±0.29,1.609±0.050),CAO조(24.55±6.25,1.844±0.027)화M조(11.60±1.21,1.733±0.027)기관TNF-α양성단위급평균흡광도(A)치균명현승고,이M조교CAO조명현강저,차이균유통계학의의(P균<0.01).ELISA결과현시:CAO조[(221.58±5.23)ng/L]화M조[(103.45±4.56)ng/L3폐조직TNF-α양성면역반응물질적표체수평균고우S조E(47.14±1.36)ng/L),차M조현저저우CAO조(P균<0.01).결론 급성심기결혈능통과신경궤제개도폐장TNF-α표체상조;아편류물질급기수체궤제삼여료궤체내심장상해성신경신호전도적조절.
Objective To investigate the expression of tumor necrosis factor-α (TNF-α) in lungs following coronary artery occlusion (CAO) and the effect of morphine pretreatment via epidural administra-tion on its expression in the rats. Methods Eighteen adult healthy male Sprague-Dawley (SD) rats were randomly divided into sham operation group (S group), CAO group and morphine pretreatment group (M group), with 6 in each group. In S group the left anterior descending branch of coronary artery was not occluded. In CAO group the left anterior descending branch of coronary artery was occluded. In M group the rats were pre-treated with morphine 60 μg/kg by epidural injection 15 minutes before CAO. The right lung was harvested 3 hours after CAO. The expression of TNF-α in lungs was assessed with immuno-histochemistry and enzyme linked immunosorbent assay (ELISA). Results The immunohistochemistry results showed, compared with S group (8. 68±0. 29, 1. 609 ± 0. 050), the positive unit and average light density of TNF-α in CAO group (24. 55±6. 25, 1. 844±0. 027) and M group (11.60±1.21, 1. 733±0. 027) were higher significantly, while they were lower significantly in M group compared with CAO group (all P<0. 01). ELISA results showed the level of TNF-α in the lung was significantly higher in CAO group [(221.58±5. 23) ng/L] and M group [(103. 45±4. 56) ng/L] than that in S group [(47. 14±1.36) ng/L],while it was significantly lower in M group compared with CAO group (all P<0. 01). Conclusion Acute myocardial ischemia could cause up-regulation of TNF-a in lungs, which is likely to be mediated by neural mechanisms. Opioid and its receptors in spinal cord might be involved in modulation of inflammatory reaction in the lung after acute coronary ischemia.
