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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45min、再灌注120min,再灌注前后静脉应用生理盐水;重组水蛭素组:缺血45min、再灌注120min,再灌注前15min静注重组水蛭素(1mg/kg),再灌注时继以持续静滴重组水蛭素犤1mg/(kg·h)犦120min。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。
BACKGROUND: Recombinant hirudin can prevent myocardial ischemia / reperfusion (IR) injury by inhibiting leukocyte infiltration, and thus play a protective role on myocardium. AIM: To observe the effect of recombinant hirudin on leukocyte infiltration in ischemic myocardium , To further explore the mechanism of recombinant hirudin on myocardial protection. Design: Randomized controlled experimental study. Location, Materials and Interventions: This experiment was performed at the Cardiovascular Disease Laboratory of Tangdu Hospital, Fourth Military Medical University. Twenty-four Japanese white rabbits were randomly divided into two groups, 12 in each group. IR group: the left anterior descending artery of the animal model of IR, ischemia 45min, reperfusion 120min, before and after reperfusion intravenous saline; recombinant hirudin group: ischemia 45min, reperfusion 120min, reperfusion 15min before intravenous injection Hirudin (1mg / kg), followed by continuous infusion of recombinant hirudin 犤 1mg / (kg · h) 再 120min after reperfusion. MAIN OUTCOME MEASURES: Changes in infarct size and leukocyte infiltration in ischemic myocardium. Results The range of myocardial infarction was (11.7 ± 2.4)% in the recombinant hirudin group compared with (21.2 ± 5.3)% in the ischemic reperfusion group (t = 7.436, P <0.01). Myeloperoxidase (MPO) activity was (56.01 ± 3.83) nkat / g in ischemic reperfusion group and 35.51 ± 1.67 nkat / g in recombinant hirudin group. The leukocyte accumulation in ischemic myocardium of recombinant hirudin group was significantly lower than that of ischemia / reperfusion group (t = 3.935, P <0.05). Conclusion: Recombinant hirudin can inhibit leukocyte infiltration in ischemic myocardium during reperfusion and antagonize myocardial IR injury.