中国临床康复
中國臨床康複
중국림상강복
CHINESE JOURNAL OF CLINICAL REHABILITATION
2004年
15期
2966-2967
,共2页
冷立娟%冷钦%杨欣国%李波%张红爱%李文联
冷立娟%冷欽%楊訢國%李波%張紅愛%李文聯
랭립연%랭흠%양흔국%리파%장홍애%리문련
心肌再灌注损伤/药物疗法%水蛭素/药理学%过氧化物酶/分析
心肌再灌註損傷/藥物療法%水蛭素/藥理學%過氧化物酶/分析
심기재관주손상/약물요법%수질소/약이학%과양화물매/분석
背景:重组水蛭素能否通过抑制白细胞浸润来拮抗心肌缺血/再灌注(ischemia/reperfusion,IR)损伤,从而起到对心肌的保护作用?目的:观察重组水蛭素对缺血心肌内白细胞浸润的影响,进一步探讨重组水蛭素对心肌保护的作用机制.设计:随机对照的实验研究.地点、材料和干预:本实验在第四军医大学唐都医院心血管病实验室完成.选取24只日本大耳白兔随机分为2组,每组12只.IR组;心脏左冠状动脉前降支IR动物模型,缺血45 min、再灌注120 min,再灌注前后静脉应用生理盐水;重组水蛭素组:缺血45 min、再灌注120 min,再灌注前15 min静注重组水蛭素(1 mg/kg),再灌注时继以持续静滴重组水蛭素[1 mg/(kg·h)]120 min.主要观察指标:心肌梗死范围及缺血心肌内白细胞浸润的变化.结果重组水蛭素组的心肌梗死范围为(11.7±2.4)%,与缺血再灌注组的(21.2±5.3)%比较,梗死范围明显缩小(t=7.436,P<0.01).缺血再灌注组的髓过氧化物酶(myeloperoxidase,MPO)活性为(56.01±3.83)nkat/g,重组水蛭素组(35.51±1.67)nkat/g.重组水蛭素组缺血心肌内白细胞聚集较缺血再灌注组显著减少(t=3.935,P<0.05).结论:重组水蛭素能够抑制再灌注期缺血心肌内白细胞浸润,拮抗心肌IR损伤.
揹景:重組水蛭素能否通過抑製白細胞浸潤來拮抗心肌缺血/再灌註(ischemia/reperfusion,IR)損傷,從而起到對心肌的保護作用?目的:觀察重組水蛭素對缺血心肌內白細胞浸潤的影響,進一步探討重組水蛭素對心肌保護的作用機製.設計:隨機對照的實驗研究.地點、材料和榦預:本實驗在第四軍醫大學唐都醫院心血管病實驗室完成.選取24隻日本大耳白兔隨機分為2組,每組12隻.IR組;心髒左冠狀動脈前降支IR動物模型,缺血45 min、再灌註120 min,再灌註前後靜脈應用生理鹽水;重組水蛭素組:缺血45 min、再灌註120 min,再灌註前15 min靜註重組水蛭素(1 mg/kg),再灌註時繼以持續靜滴重組水蛭素[1 mg/(kg·h)]120 min.主要觀察指標:心肌梗死範圍及缺血心肌內白細胞浸潤的變化.結果重組水蛭素組的心肌梗死範圍為(11.7±2.4)%,與缺血再灌註組的(21.2±5.3)%比較,梗死範圍明顯縮小(t=7.436,P<0.01).缺血再灌註組的髓過氧化物酶(myeloperoxidase,MPO)活性為(56.01±3.83)nkat/g,重組水蛭素組(35.51±1.67)nkat/g.重組水蛭素組缺血心肌內白細胞聚集較缺血再灌註組顯著減少(t=3.935,P<0.05).結論:重組水蛭素能夠抑製再灌註期缺血心肌內白細胞浸潤,拮抗心肌IR損傷.
배경:중조수질소능부통과억제백세포침윤래길항심기결혈/재관주(ischemia/reperfusion,IR)손상,종이기도대심기적보호작용?목적:관찰중조수질소대결혈심기내백세포침윤적영향,진일보탐토중조수질소대심기보호적작용궤제.설계:수궤대조적실험연구.지점、재료화간예:본실험재제사군의대학당도의원심혈관병실험실완성.선취24지일본대이백토수궤분위2조,매조12지.IR조;심장좌관상동맥전강지IR동물모형,결혈45 min、재관주120 min,재관주전후정맥응용생리염수;중조수질소조:결혈45 min、재관주120 min,재관주전15 min정주중조수질소(1 mg/kg),재관주시계이지속정적중조수질소[1 mg/(kg·h)]120 min.주요관찰지표:심기경사범위급결혈심기내백세포침윤적변화.결과중조수질소조적심기경사범위위(11.7±2.4)%,여결혈재관주조적(21.2±5.3)%비교,경사범위명현축소(t=7.436,P<0.01).결혈재관주조적수과양화물매(myeloperoxidase,MPO)활성위(56.01±3.83)nkat/g,중조수질소조(35.51±1.67)nkat/g.중조수질소조결혈심기내백세포취집교결혈재관주조현저감소(t=3.935,P<0.05).결론:중조수질소능구억제재관주기결혈심기내백세포침윤,길항심기IR손상.
BACKGROUND: It is not very clear that recombinant hirudin(r-hirudin)can inhibit the ueutrophil infiltration against myocardial ischemia-reperfusion(IR) injury.OBJECTIVE: To observe the effect of r-hirudin on the accumulation of neutrophils in ischemic cardiac tissues and investigate its protective mechanism against myocardial IR injury in rabbits.DESIGN: A randomly controlled experimental study.SETTING, PARTICIPANTS and INTERVENTIONS: The experiment was performed at the institute of cardiovascular disease research of Tangdu Hospital, Fourth Military Medical University of Chinese PLA. A total of 24 rabbits were randomly divided into ischemia-reperfusion (IR) group ( n = 12) and r-hirudin group ( n = 12). In the IR group the left anterior descending coronary artery was occluded for 45 minutes followed by 120 minutes reperfusion, and saline was infused before and during reperfusion. In the r-hirudin group, the operation on rabbits was the same as IR group and r-hirudin treatment began with the intravenous administration of 1 mg/kg 15 minutes before reperfusion,following reperfusion.MAIN OUTCOME MEASURES: Changes of the infarct size and the neutrophil infiltration in ischemic cardiac tissues were observed.RESULTS: R-hirudin resulted in a significant reduction in the infarct size with respect to rabbits in IR group [(11.7±2.4)% vs (21.2±5.3%)]( t = 7.436, P < 0.01 ). The MPO activity was (56.01 ± 3.83)nkat/g and (35.51 ± 1.67) nkat/g respectively in the r-hirudin and IR groups. In the r-hirudin group, the neutrophil infiltration in ischemie cardiac tissues was significantly decreased in comparison with that in the IR group ( t = 3.935,P <0.05).CONCLUSION: R-hirudin has the cardioprotective action against myocardial IR injury by inhibiting neutrophil infiltration in ischemic myocardial tissues.