CAJ | 학술논문

目的观察缺血前预处理对机体内一氧化氮(NO)表达的影响.方法选择成年健康Wistar沙土鼠50只,建立离体Langendorff灌流模型,按照缺血前处理方法的不同平分为5组,正常对照组选择恒压灌流105 min;缺血再灌注组进行平衡20 min,停灌45 min后再灌注60 min;预处理组在停灌45 min后,再灌注60 min前给予6个循环的30 s缺血(R)/30 s再灌注(Ⅰ);预处理+依达拉奉组或丹参组使用含依达拉奉或丹参的灌流液于停灌前灌注10 min,并至再灌注结束.结果正常对照组、缺血再灌注组、预处理组、预处理+依达拉奉组与预处理+丹参组在灌注60 min时冠脉流出液中的乳酸脱氢酶(LDH)活性分别为(352.12±9.63)、(615.36±66.36)、(473.19±50.18)、(412.39±35.48)、(399.54±45.89) mU.与正常对照组比较,缺血再灌注组再灌注60 min时冠脉流出液中LDH活性显著升高(P＜0.05),而预处理能显著降低冠脉流出液中LDH酶活性(P＜0.05).正常对照组苏木素-伊红(HE)染色显示心肌细胞有序排列,无炎性细胞浸润;缺血再灌注组心肌细胞排列杂乱,细胞肿胀,有少量炎性细胞浸润;预处理3组的细胞损害程度明显低于缺血再灌注组.与正常对照组比较,再灌注60 min后缺血再灌注组心肌组织内NO含量与总一氧化氮合酶(TNOS)和诱导型一氧化氮合酶(iNOS)活性显著升高(P＜0.05),而预处理能显著降低心肌组织内NO含量与TNOS和iNOS活性(P＜0.05);依达拉奉与丹参的处理使预处理对心肌组织内上述指标的降低作用更显著(P＜0.05).结论缺血前预处理可减少离体培养心肌组织的LDH释放,从而表现出对心肌细胞的保护作用,该作用可能是通过对NO-iNOS信号通路进行调节而实现的,依达拉奉与丹参的应用能更加有效发挥预处理作用.
목적 관찰결혈전예처리대궤체내일양화담(NO)표체적영향.방법 선택성년건강Wistar사토서50지,건립리체Langendorff관류모형,안조결혈전처리방법적불동평분위5조,정상대조조선택항압관류105 min;결혈재관주조진행평형20 min,정관45 min후재관주60 min;예처리조재정관45 min후,재관주60 min전급여6개순배적30 s결혈(R)/30 s재관주(Ⅰ);예처리+의체랍봉조혹단삼조사용함의체랍봉혹단삼적관류액우정관전관주10 min,병지재관주결속.결과 정상대조조、결혈재관주조、예처리조、예처리+의체랍봉조여예처리+단삼조재관주60 min시관맥류출액중적유산탈경매(LDH)활성분별위(352.12±9.63)、(615.36±66.36)、(473.19±50.18)、(412.39±35.48)、(399.54±45.89) mU.여정상대조조비교,결혈재관주조재관주60 min시관맥류출액중LDH활성현저승고(P＜0.05),이예처리능현저강저관맥류출액중LDH매활성(P＜0.05).정상대조조소목소-이홍(HE)염색현시심기세포유서배렬,무염성세포침윤;결혈재관주조심기세포배렬잡란,세포종창,유소량염성세포침윤;예처리3조적세포손해정도명현저우결혈재관주조.여정상대조조비교,재관주60 min후결혈재관주조심기조직내NO함량여총일양화담합매(TNOS)화유도형일양화담합매(iNOS)활성현저승고(P＜0.05),이예처리능현저강저심기조직내NO함량여TNOS화iNOS활성(P＜0.05);의체랍봉여단삼적처리사예처리대심기조직내상술지표적강저작용경현저(P＜0.05).결론 결혈전예처리가감소리체배양심기조직적LDH석방,종이표현출대심기세포적보호작용,해작용가능시통과대NO-iNOS신호통로진행조절이실현적,의체랍봉여단삼적응용능경가유효발휘예처리작용.
Objective To investigate the effects of ischemic pretreatment on the expression of nitric oxide (NO) in vivo.Methods Fifty adult healthy Wistar gerbils were selected,there were established in vitro Langendorff perfusion model,accorded to different levels of ischemic pre-treatment methods were equally divided into 5 groups (the normal control group were selected constant perfusion 105 min; ischemia; And the reperfusion group were balance 20 min,45 min after stopping irrigation irrigation 60 min; The pretreatment group were 45 min after stopping irrigation,60 min before reperfusion given six cycles 30 s R/30 s Ⅰ; The pretreatment + edaravone group and the pretreatment + salvia group were used the Salvia edaravone or salvia perfusion perfusion 10 min before stopping irrigation.Results The coronary effluent lactate dehydrogenase (LDH) activity in the six groups were (352.12 ± 9.63),(615.36 ± 66.36),(473.19 ± 50.18),(412.39 ± 35.48),(399.54 ± 45.89) mU,Compared with normal control group,the coronary effluent LDH activity in the ischemia-reperfusion group 60 min reperfusion were significantly increased (P ＜ 0.05),whereas the pretreatment can significantly reduce coronary effluent LDH activity (P ＜ 0.05).Hematoxylin and eosin (HE) staining showed that the normal control group were ordered myocardial cells and were no inflammatory cell infiltration; The myocardial ischemia-reperfusion group were showed arranged clutter,cell swelling and were small amount of inflammatory cell infiltration; The pretreatment were showed damage were significantly lower than the ischemic reperfusion group.Compared with normal control group,reperfusion within 60 min after myocardial,the NO content and total nitric oxide synthase (TNOS),inducible nitric oxide synthase (iNOS) activity of the ischemia-reperfusion group were significantly increased (P ＜0.05),whereas pretreatment can significantly reduce NO content and TNOS iNOS activity in the myocardial tissue (P ＜ 0.05) ; The edaravone and salvia treatment can reduce the NO content and TNOS iNOS activity in the myocardial tissue (P ＜ 0.05).Conclusion Ischemic preconditioning can reduce lactate dehydrogenase release in the myocardial tissue,thus it showed the protective effect on myocardial cells,which it may be through the NO-iNOS signaling pathways regulate,Edaravone and Salvia applications can play more effective role in the pretreatment.