中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2009年
8期
700-703
,共4页
王丽%严虹%李建国%朱学敏%吴若岚%蔡毅
王麗%嚴虹%李建國%硃學敏%吳若嵐%蔡毅
왕려%엄홍%리건국%주학민%오약람%채의
胆碱能药%心肌再灌注损伤
膽堿能藥%心肌再灌註損傷
담감능약%심기재관주손상
Cholinergic agents%Myocardial reperfusion injury
目的 探讨烟碱对大鼠心肌缺血再灌注损伤的影响.方法 健康成年雄性SD大鼠74只,体重200～250 g,随机分为5组:假手术组(S组,n=10)、缺血再灌注组(IR组,n=16)、烟碱400 μg/kg组(N1组,n=16)、烟碱40 μg/kg组(N2组,n=16)和α-银环蛇毒素组(α-BGT组,n=16).S组只穿线,不结扎左冠状动脉前降支;余各组采用结扎左冠状动脉前降支30 min,再灌注60 min的方法 制备大鼠心肌缺血再灌注模型.缺血前30 min时,N1组和N2组经右颈静脉分别注射烟碱400和40 μg/kg,α-BGT组右颈静脉注射N型胆碱能受体α-7亚单位特异性阻断剂α-银环蛇毒素1.0 μg/kg+烟碱400 μg/kg,S组和IR组右颈静脉注射等量生理盐水.再灌注60 min时,IR组、N1组、N2组和α-BGT组各取6只大鼠,测定左心室面积(LVA)、缺血危险区面积(AAR)和梗死区面积(IA),计算AAR/LVA和IA/LVA.再灌注60 min时,各组取10只大鼠,采集右颈动脉血样,测定血浆肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)的浓度和肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)的活性;然后处死动物,取心肌组织,观察心肌超微结构,测定心肌髓过氧化物酶(MPO)活性.结果 与S组比较,IR组、N1组、N2组、α-BGT组血浆 TNF-α、IL-1β的浓度和CK-MB、LDH的活性升高,心肌MFO活性升高(P<0.05);与IR组比较,N1组IA/LVA、血浆TNF-α、IL-1β的浓度和CK-MB、LDH的活性、心肌MPO活性降低(P<0.05),心肌细胞超微结构损伤减轻,N2组和α-BGT组上述指标差异无统计学意义(P>0.05);与N1组比较,N2组和α-BGT组IA/LVA、血浆TNF-α、IL-1β的浓度和CK-MB、LDH的活性、心肌MPO活性升高(P<0.05),心肌细胞超微结构损伤加重.结论 烟碱可减轻大鼠心肌缺血再灌注损伤,其机制可能与激活胆碱能抗炎通路,抑制炎性反应有关.
目的 探討煙堿對大鼠心肌缺血再灌註損傷的影響.方法 健康成年雄性SD大鼠74隻,體重200～250 g,隨機分為5組:假手術組(S組,n=10)、缺血再灌註組(IR組,n=16)、煙堿400 μg/kg組(N1組,n=16)、煙堿40 μg/kg組(N2組,n=16)和α-銀環蛇毒素組(α-BGT組,n=16).S組隻穿線,不結扎左冠狀動脈前降支;餘各組採用結扎左冠狀動脈前降支30 min,再灌註60 min的方法 製備大鼠心肌缺血再灌註模型.缺血前30 min時,N1組和N2組經右頸靜脈分彆註射煙堿400和40 μg/kg,α-BGT組右頸靜脈註射N型膽堿能受體α-7亞單位特異性阻斷劑α-銀環蛇毒素1.0 μg/kg+煙堿400 μg/kg,S組和IR組右頸靜脈註射等量生理鹽水.再灌註60 min時,IR組、N1組、N2組和α-BGT組各取6隻大鼠,測定左心室麵積(LVA)、缺血危險區麵積(AAR)和梗死區麵積(IA),計算AAR/LVA和IA/LVA.再灌註60 min時,各組取10隻大鼠,採集右頸動脈血樣,測定血漿腫瘤壞死因子α(TNF-α)、白細胞介素1β(IL-1β)的濃度和肌痠激酶同工酶(CK-MB)、乳痠脫氫酶(LDH)的活性;然後處死動物,取心肌組織,觀察心肌超微結構,測定心肌髓過氧化物酶(MPO)活性.結果 與S組比較,IR組、N1組、N2組、α-BGT組血漿 TNF-α、IL-1β的濃度和CK-MB、LDH的活性升高,心肌MFO活性升高(P<0.05);與IR組比較,N1組IA/LVA、血漿TNF-α、IL-1β的濃度和CK-MB、LDH的活性、心肌MPO活性降低(P<0.05),心肌細胞超微結構損傷減輕,N2組和α-BGT組上述指標差異無統計學意義(P>0.05);與N1組比較,N2組和α-BGT組IA/LVA、血漿TNF-α、IL-1β的濃度和CK-MB、LDH的活性、心肌MPO活性升高(P<0.05),心肌細胞超微結構損傷加重.結論 煙堿可減輕大鼠心肌缺血再灌註損傷,其機製可能與激活膽堿能抗炎通路,抑製炎性反應有關.
목적 탐토연감대대서심기결혈재관주손상적영향.방법 건강성년웅성SD대서74지,체중200～250 g,수궤분위5조:가수술조(S조,n=10)、결혈재관주조(IR조,n=16)、연감400 μg/kg조(N1조,n=16)、연감40 μg/kg조(N2조,n=16)화α-은배사독소조(α-BGT조,n=16).S조지천선,불결찰좌관상동맥전강지;여각조채용결찰좌관상동맥전강지30 min,재관주60 min적방법 제비대서심기결혈재관주모형.결혈전30 min시,N1조화N2조경우경정맥분별주사연감400화40 μg/kg,α-BGT조우경정맥주사N형담감능수체α-7아단위특이성조단제α-은배사독소1.0 μg/kg+연감400 μg/kg,S조화IR조우경정맥주사등량생리염수.재관주60 min시,IR조、N1조、N2조화α-BGT조각취6지대서,측정좌심실면적(LVA)、결혈위험구면적(AAR)화경사구면적(IA),계산AAR/LVA화IA/LVA.재관주60 min시,각조취10지대서,채집우경동맥혈양,측정혈장종류배사인자α(TNF-α)、백세포개소1β(IL-1β)적농도화기산격매동공매(CK-MB)、유산탈경매(LDH)적활성;연후처사동물,취심기조직,관찰심기초미결구,측정심기수과양화물매(MPO)활성.결과 여S조비교,IR조、N1조、N2조、α-BGT조혈장 TNF-α、IL-1β적농도화CK-MB、LDH적활성승고,심기MFO활성승고(P<0.05);여IR조비교,N1조IA/LVA、혈장TNF-α、IL-1β적농도화CK-MB、LDH적활성、심기MPO활성강저(P<0.05),심기세포초미결구손상감경,N2조화α-BGT조상술지표차이무통계학의의(P>0.05);여N1조비교,N2조화α-BGT조IA/LVA、혈장TNF-α、IL-1β적농도화CK-MB、LDH적활성、심기MPO활성승고(P<0.05),심기세포초미결구손상가중.결론 연감가감경대서심기결혈재관주손상,기궤제가능여격활담감능항염통로,억제염성반응유관.
Objective To investigate the effects of nicotine on myocardial iscbemia-reperfusion (IR) injury in rats. Methods Seventy-four male SD rats weighing 200-250 g were randomly divided into 5 groups: group Ⅰ sham operation (group S, n=10), group Ⅱ IR (n = 16), group Ⅲ nicotine 400 μg/kg (group N1,n = 16), group Ⅳ nicotine 40 μg/kg (group N2, n = 16) and group Ⅴ nicotine 400 μg/kg + a-bungarotoxin(group a-BGT, n = 16). Myocardial ischemia was induced by occlusion of left anterior descending branch (LAD) of coronary artery for 30 min followed by 60 min of reperfusiou. LAD was exposed, but not occluded in group S. Nicotine 400 and 40 μg/kg were injected iv via the right jugular vein in group N1 and N2 respectively, and a-bungarotoxin 1.0 μg/kg and nicotion 400 μg/kg were injected iv via the fight jugular vein in group a-BGT at 30 min before myocardial ischemia. Equal volume of normal saline was injected instead in group S and IR. Six animals in each group were killed at 60 min of reperfusion and the hearts removed to measure the left ventricular area (LVA), area at risk (MR) and infarct area (IA) in group IR, N1,N2 and α-BGT. AAP/LVA and IA/LVA were calculated. The blood samples from right carotid artery were obtained for determination of plasma concentrations of TNF-α and IL-1β and activities of CK-MB and LDH. The animals were then killed and the hearts removed to observe the myocardial ultrastrueture and determine the activity of MPO. Results Compared with group S, plasma concentrations of TNF-α and IL-1β and activities of CK-MB and LDH, and myocardial MPO activity were significantly increased in group IR, N1, N2 and a-BGT (P<0.05). Compared with group IB, IA/LVA,plasma concentrations of TNF-α and IL-1β and activities of CK-MB and LDH, and myocardial MPO activity were significantly decreased in group N1 (P < 0.05), but there was no significant difference in the indices mentioned above between group N2 and IB and between group α-BGT and IB (P > 0.05). Compared with group N1,IA/LVA, plasma concentrations of TNF-α and IL-1βand activities of CK-MB and LDH, and myocardial MPO activity were significantly increased in group N2 and α-BGT (P < 0.05). The injury to myocardial uhrastructure was attenuated in group N1 as compared with group IR, while aggravated in group N2 and α-BGT as compared with group N1. Conclusion Nicotine can ameliorate the myocardial IR in rats. The mechanism may be related to the activation of the cholinergic anti-inflanunatory pathway and inhibition of the inflammatory response.
