中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2010年
5期
420-423
,共4页
李敏%张健%梁艳虹%陈艳蓉%王梦然%肖瑶%宿慧
李敏%張健%樑豔虹%陳豔蓉%王夢然%肖瑤%宿慧
리민%장건%량염홍%진염용%왕몽연%초요%숙혜
缺血预处理,心肌%心肌梗死%心肌再灌注损伤%蛋白激酶C
缺血預處理,心肌%心肌梗死%心肌再灌註損傷%蛋白激酶C
결혈예처리,심기%심기경사%심기재관주손상%단백격매C
Ischemic postconditioning,myocardial%Myocardial infarction%Reperfusion injury%Protein kinase C
目的 研究心肌缺血后处理对老年大鼠急性心肌缺血再灌注损伤后心肌梗死面积、心肌细胞蛋白激酶Cα(PKCα)表达的影响,并探讨其可能机制.方法 120只健康雄性Wistar大鼠,根据鼠龄分为老年和成年组,每组再分为对照组(缺血30 min再灌注3 h,12只)和5 s、10 s、30 s、60 s组(缺血30 min,再灌注开始时分别给予5 s、10 s、30 s、60 s再通-闭塞冠状动脉处理后再灌注共3 h,每组12只).2,3,5-三苯基氯化四氮唑染色测定心肌梗死面积,免疫组化技术检测心肌细胞PKCα表达.结果 不同时间缺血处理心肌梗死面积和PKCα表达不同,对照组、10 s和30 s再通-闭塞处理均可缩小老年和成年大鼠心肌梗死面积[分别为(55.9±6.0)%和(47.4±5.5)%、(48.1±5.3)%、和(39.2±5.7)%、(48.8±6.8)%和(40.2±6.1)%],PKCα表达增加(均P<0.05);老年5 s组再通-闭塞处理可增加大鼠心肌梗死面积,老年5 s组梗死面积为(63.5±5.4)%,PKCα表达降低(均P<0.05).结论 缺血后处理对老年大鼠急性心肌缺血再灌注损伤具有保护作用;缺血后处理效果与再通-闭塞时间有关.
目的 研究心肌缺血後處理對老年大鼠急性心肌缺血再灌註損傷後心肌梗死麵積、心肌細胞蛋白激酶Cα(PKCα)錶達的影響,併探討其可能機製.方法 120隻健康雄性Wistar大鼠,根據鼠齡分為老年和成年組,每組再分為對照組(缺血30 min再灌註3 h,12隻)和5 s、10 s、30 s、60 s組(缺血30 min,再灌註開始時分彆給予5 s、10 s、30 s、60 s再通-閉塞冠狀動脈處理後再灌註共3 h,每組12隻).2,3,5-三苯基氯化四氮唑染色測定心肌梗死麵積,免疫組化技術檢測心肌細胞PKCα錶達.結果 不同時間缺血處理心肌梗死麵積和PKCα錶達不同,對照組、10 s和30 s再通-閉塞處理均可縮小老年和成年大鼠心肌梗死麵積[分彆為(55.9±6.0)%和(47.4±5.5)%、(48.1±5.3)%、和(39.2±5.7)%、(48.8±6.8)%和(40.2±6.1)%],PKCα錶達增加(均P<0.05);老年5 s組再通-閉塞處理可增加大鼠心肌梗死麵積,老年5 s組梗死麵積為(63.5±5.4)%,PKCα錶達降低(均P<0.05).結論 缺血後處理對老年大鼠急性心肌缺血再灌註損傷具有保護作用;缺血後處理效果與再通-閉塞時間有關.
목적 연구심기결혈후처리대노년대서급성심기결혈재관주손상후심기경사면적、심기세포단백격매Cα(PKCα)표체적영향,병탐토기가능궤제.방법 120지건강웅성Wistar대서,근거서령분위노년화성년조,매조재분위대조조(결혈30 min재관주3 h,12지)화5 s、10 s、30 s、60 s조(결혈30 min,재관주개시시분별급여5 s、10 s、30 s、60 s재통-폐새관상동맥처리후재관주공3 h,매조12지).2,3,5-삼분기록화사담서염색측정심기경사면적,면역조화기술검측심기세포PKCα표체.결과 불동시간결혈처리심기경사면적화PKCα표체불동,대조조、10 s화30 s재통-폐새처리균가축소노년화성년대서심기경사면적[분별위(55.9±6.0)%화(47.4±5.5)%、(48.1±5.3)%、화(39.2±5.7)%、(48.8±6.8)%화(40.2±6.1)%],PKCα표체증가(균P<0.05);노년5 s조재통-폐새처리가증가대서심기경사면적,노년5 s조경사면적위(63.5±5.4)%,PKCα표체강저(균P<0.05).결론 결혈후처리대노년대서급성심기결혈재관주손상구유보호작용;결혈후처리효과여재통-폐새시간유관.
Objective To observe the effects of ischemic postconditioning (IPTC) on myocardial infarction sizes (IS) and protein kinase Cα (PKCα) expression in aged rats with post-ischemia reperfusion injury,and to explore the mechanism.Methods A total of 120 male Wistar rats were divided into aged group and adult group.The aged group was randomly divided into control group (n=12,30-min ischemia and 3-h reperfusion),5 s,10 s,30 s and 60 s IPTC groups [n= 12,each;after 30 min occlusion of left coronary artery (LCA),three cycles of 5 s,10 s,30 s,60 s reperfusion respectively followed by the same interval LCA re-occlusion were applied at the beginning of reperfusion].The IS was measured with TTC dye,and PKC expression was investigated by immunohistochemistry.Results Different IPTC intervals had different effects on IS and PKC expression,10 s and 30 s IPTC could reduce IS both in aged rats and adult rats [(55.9±6.0)% and (47.4±5.5)%],IS in 10 s IPTC group in aged rats was (48.1±5.3)%,in adult rats was (39.2±5.7) %;IS in 30 s IPTC group in aged rats was (48.8 ± 6.8) %,in adult rats was (40.2 ± 6.1 ) %.PKCα expression increased in aged and adult rats (all P<0.05).5 s IPTC could increase IS [IS in 5 s IPTC group in aged rats was (63.5±5.4)%,and PKCα expression reduced in aged rats (all P<0.05)].Conclusions IPTC has cardio-protective effect in aged rats suffering from acute myocardial injury during reperfusion,the effect of IPTC is related to reperfusion-reocclusion interval.
