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大白兔冠状动脉微血栓模型的建立
引用本文:陈良,蒋锦琪,张道良.大白兔冠状动脉微血栓模型的建立[J].临床心血管病杂志,2012(1):76-79.
作者姓名:陈良  蒋锦琪  张道良
作者单位:上海交通大学附属胸科医院急诊科
摘    要:目的:建立新西兰大白兔冠状动脉微血栓的模型,探讨其机制。方法:取新西兰大白兔45只,随机分为模型组(20只)、假手术组(20只)和对照组(5只)。开胸后阻断升主动脉10s,模型组经主动脉根部注入月桂酸钠1.5mg/kg(浓度为40mg/ml),假手术组注入相同体积0.9%氯化钠溶液,对照组不做任何处理。于术后1、3、24、72h分别取心脏病理检测,各时间点各取5只大白兔,每个心脏取5张切片,观察各组微血栓形成情况、计算血栓形成率。于术前和术后3h各采血2ml,测定、比较血清一氧化氮(NO)、内皮素-1(ET-1)和血管内皮生长因子(VEGF)浓度。结果:模型组在注入月桂酸钠后1h微血栓形成率为(8.49±3.12)%,于注射后3h(24.21±6.52)%]达高峰,24h(16.65±5.84)%]和72h(9.87±3.55)%]后逐渐减少,各时间点差异有统计学意义(P<0.05)。与对照组比较,模型组NO下降(7.30±0.86)μmol/L∶(3.49±0.81)μmol/L,P<0.01],ET-1上升(17.83±1.89)pg/ml∶(29.21±2.19)pg/ml,P<0.01],VEGF上升(96.74±11.06)pg/ml∶(145.20±11.12)pg/ml,P<0.01]。结论:用月桂酸钠(经主动脉)行冠状动脉内注射能成功地建立新西兰大白兔冠状动脉微血栓模型,其最佳剂量和时间点为1.5mg/kg和术后3h,其主要机制为月桂酸钠导致了冠状动脉微血管内皮损伤和(或)功能障碍。

关 键 词:冠状动脉  月桂酸钠  微血栓  模型

Establishment of coronary microthrombosis model in white rabbits
CHEN Liang,JIANG Jinqi,ZHANG Daoliang.Establishment of coronary microthrombosis model in white rabbits[J].Journal of Clinical Cardiology,2012(1):76-79.
Authors:CHEN Liang  JIANG Jinqi  ZHANG Daoliang
Institution:(Emergency Department,Shanghai Chest Hospital Affiliated to Shanghai Jiaotong University,Shanghai,200030,China)
Abstract:Objective:To establish a new coronary microthrombosis model in New Zealand white rabbits,and to investigate the mechanism.Method:A total of 45 rabbits were divided into model group(n=20),sham operation group(n=20) and control group(n=5) randomly. In model group,sodium laurate was injected into aortic root by dose of 1.5 mg/kg and by concentration of 40 mg/ml,while in sham operation group,the same volume of saline was injected into aortic root,with aortic clamping for 10 s.Nothing was done in control group.The heart specimens were obtained at 1 h,3 h,24 h and 72 h after sodium laurate injection,and 5 slides were taken in each heart specimen to observe the formation of microthrombus and to calculate the number of thrombus.There were 5 rabbits at each time point,respectively.At the same time,2 ml blood was taken at 0 and 3 h after sodium laurate injection in each operation group to determine the serum concentration of NO,ET-1 and VEGF.Result:The formation of microthrombus in model group was(8.49±3.12)% at 1 h after sodium laurate injection,got its highest level at 3 h(24.21±6.52)%,and decreased at 24 h(16.65±5.84)% and 72 h(9.87±3.55)%,P<0.05.Compared with control group,the concentration of NO in model group decreased(7.30±0.86]μmol/L vs 3.49±0.81]μmol/L,P<0.01),ET-1 increased(17.83±1.89]pg/ml vs 29.21±2.19]pg/ml,P<0.01) and VEGF increased(96.74±11.06]pg/ml vs 145.20±11.12]pg/ml,P<0.01) significantly.Conclusion:We can establish a new coronary microthrombosis model in New Zealand white rabbits by injecting sodium laurate into coronary artery from aortic root.Its optimal dose and time point were 1.5 mg/kg and 3 h after operation.The mechanism of the formation of microthrombus was the injury and/or dysfunction of coronary microvascular endothelium caused by sodium laurate.
Keywords:coronary artery disease  sodium laurate  microthrombus  model
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