中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2013年
3期
363-365
,共3页
刘薇%严虹%王丽%陈璟莉%严启韬%吴若岚
劉薇%嚴虹%王麗%陳璟莉%嚴啟韜%吳若嵐
류미%엄홍%왕려%진경리%엄계도%오약람
胆碱能药%心肌再灌注损伤%心脏功能试验
膽堿能藥%心肌再灌註損傷%心髒功能試驗
담감능약%심기재관주손상%심장공능시험
Cholinergic Agents%Myocardial reperfusion injury%Heart function tests
目的 评价烟碱预先给药对心肌缺血再灌注大鼠心功能的影响.方法 健康成年雄性SD大鼠60只,体重200 ~ 250 g,采用随机数字表法,将其分为3组(n=20)∶假手术组(S组)、心肌缺血再灌注组(IR组)和烟碱预先给药组(N组).S组丝线穿过冠状动脉前降支但不结扎;IR组采用丝线结扎左冠状动脉前降支30 min后再灌注120 min的方法制备大鼠心肌缺血再灌注模型.N组结扎前30 min,经右颈静脉注射烟碱400μg/kg,余操作同IR组,S组和IR组右颈静脉注射等量生理盐水.各组随机取10只大鼠于缺血前(T0)、缺血30 min(T1)和再灌注30 min(T2)、120 min(T3)时经生物机能实验系统记录左心室收缩压(LVSP)、左心室舒张压(LVDP)、左室内压上升/下降最大变化速率(±dp/dtmax)、HR和MAP.各组其余10只大鼠于再灌注60 min时采集右颈动脉血样,采用ELISA法测定血浆肌酸激酶同工酶(CK-MB)活性、心肌肌钙蛋白I(cTnI)和TNF-α浓度.结果 与S组比较,IR组T23时MAP和LVSP、T13时HR、LVDP和±dp/dtmax降低,血浆CK-MB活性、cTnI和TNF-α浓度升高,N组T1-2时LVDP、T1-3时HR和±dp/dtmax降低,血浆CK-MB活性、cTnI和TNF-α浓度升高(P<0.05);与IR组比较,N组T3时MAP、HR、LVSP、LVDP和±dp/dtmax升高,血浆CK-MB活性、cTnI和TNF-α浓度降低(P<0.05).结论 烟碱预先给药通过激活胆碱能抗炎通路,抑制炎性反应,可显著减轻大鼠心肌缺血再灌注损伤,从而改善心功能.
目的 評價煙堿預先給藥對心肌缺血再灌註大鼠心功能的影響.方法 健康成年雄性SD大鼠60隻,體重200 ~ 250 g,採用隨機數字錶法,將其分為3組(n=20)∶假手術組(S組)、心肌缺血再灌註組(IR組)和煙堿預先給藥組(N組).S組絲線穿過冠狀動脈前降支但不結扎;IR組採用絲線結扎左冠狀動脈前降支30 min後再灌註120 min的方法製備大鼠心肌缺血再灌註模型.N組結扎前30 min,經右頸靜脈註射煙堿400μg/kg,餘操作同IR組,S組和IR組右頸靜脈註射等量生理鹽水.各組隨機取10隻大鼠于缺血前(T0)、缺血30 min(T1)和再灌註30 min(T2)、120 min(T3)時經生物機能實驗繫統記錄左心室收縮壓(LVSP)、左心室舒張壓(LVDP)、左室內壓上升/下降最大變化速率(±dp/dtmax)、HR和MAP.各組其餘10隻大鼠于再灌註60 min時採集右頸動脈血樣,採用ELISA法測定血漿肌痠激酶同工酶(CK-MB)活性、心肌肌鈣蛋白I(cTnI)和TNF-α濃度.結果 與S組比較,IR組T23時MAP和LVSP、T13時HR、LVDP和±dp/dtmax降低,血漿CK-MB活性、cTnI和TNF-α濃度升高,N組T1-2時LVDP、T1-3時HR和±dp/dtmax降低,血漿CK-MB活性、cTnI和TNF-α濃度升高(P<0.05);與IR組比較,N組T3時MAP、HR、LVSP、LVDP和±dp/dtmax升高,血漿CK-MB活性、cTnI和TNF-α濃度降低(P<0.05).結論 煙堿預先給藥通過激活膽堿能抗炎通路,抑製炎性反應,可顯著減輕大鼠心肌缺血再灌註損傷,從而改善心功能.
목적 평개연감예선급약대심기결혈재관주대서심공능적영향.방법 건강성년웅성SD대서60지,체중200 ~ 250 g,채용수궤수자표법,장기분위3조(n=20)∶가수술조(S조)、심기결혈재관주조(IR조)화연감예선급약조(N조).S조사선천과관상동맥전강지단불결찰;IR조채용사선결찰좌관상동맥전강지30 min후재관주120 min적방법제비대서심기결혈재관주모형.N조결찰전30 min,경우경정맥주사연감400μg/kg,여조작동IR조,S조화IR조우경정맥주사등량생리염수.각조수궤취10지대서우결혈전(T0)、결혈30 min(T1)화재관주30 min(T2)、120 min(T3)시경생물궤능실험계통기록좌심실수축압(LVSP)、좌심실서장압(LVDP)、좌실내압상승/하강최대변화속솔(±dp/dtmax)、HR화MAP.각조기여10지대서우재관주60 min시채집우경동맥혈양,채용ELISA법측정혈장기산격매동공매(CK-MB)활성、심기기개단백I(cTnI)화TNF-α농도.결과 여S조비교,IR조T23시MAP화LVSP、T13시HR、LVDP화±dp/dtmax강저,혈장CK-MB활성、cTnI화TNF-α농도승고,N조T1-2시LVDP、T1-3시HR화±dp/dtmax강저,혈장CK-MB활성、cTnI화TNF-α농도승고(P<0.05);여IR조비교,N조T3시MAP、HR、LVSP、LVDP화±dp/dtmax승고,혈장CK-MB활성、cTnI화TNF-α농도강저(P<0.05).결론 연감예선급약통과격활담감능항염통로,억제염성반응,가현저감경대서심기결혈재관주손상,종이개선심공능.
Objective To evaluate the effect of nicotine pretreatment on cardiac function following myocardial ischemia-reperfusion (I/R) in rats.Methods Sixty male Sprague-Dawley rats,weighing 200-250 g,were randomly divided into 3 groups (n =20 each):sham operation group (group S),group I/R and nicotine pretreatment group (group N).The rats were anesthetized with intraperitoneal 20% urethane 1 g/kg,tracheostomized and mechanically ventilated.Myocardial ischemia was induced by occlusion of the left anterior descending branch of coronary artery for 30 min followed by 120 min of reperfusion.The left anterior descending branch of coronary artery was only exposed,but not occluded in group S.Nicotine 400 μg/kg was injected intravenously via the right jugular vein at 30 min before myocardial ischemia in group N.The equal volume of normal saline was injected instead in groups S and I/R.Before ischemia,at 30 min of ischemia and at 30 and 120 min of reperfusion,10 rats from each group were chosen for record of left ventricular systolic pressure (LVSP),left ventricular diastolic pressure (LVDP),± dp/dtmax,HR and mean arterial pressure (MAP).Blood samples were collected from the right carotid artery of the left 10 rats in each group at 60 min of reperfusion to measure plasma CK-MB activity and cTnI and TNF-α concentrations.Results Compared with group S,MAP and LVSP at T2,3 and HR,LVDP and ± dp/dtmax at T1-3 were significantly decreased,and the plasma CK-MB activity and cTnI and TNF-α concentrations were increased in group I/R,and LVDP at T1,2 and HR and ± dp/dtmax at T1-3 were significantly decreased,and the plasma CK-MB activity and cTnI and TNF-α concentrations were increased in group N (P < 0.05).Compared with group I/R,MAP,HR,LVSP,LVDP and ± dp/dtmax were significantly increased at T3,and the plasma CK-MB activity and cTnI and TNF-α concentrations were decreased in group N (P < 0.05).Conclusion Nicotine pretreatment can reduce myocardial I/R injury through activating cholinergic anti-inflammatory pathway,thus improving cardiac function in rats.