吸入一氧化氮对急性大面积肺血栓栓塞家兔心肌肌钙蛋白和肺动脉平均压的影响  

Effect of inhalation nitric oxide on cardiac troponin I and pulmonary arterial pressure of rabbits with acute massive pulmonary embolism

作　　者：张泽明[1] 王彦存[1] 尹娟[1] 李峥[1] 赵学琴[1] 

机构地区：[1]河北大学附属医院呼吸科,河北保定071000

出　　处：《中国现代医学杂志》2010年第5期667-671,共5页China Journal of Modern Medicine

摘　　要：目的:通过建立大面积肺血栓栓塞症心肌受损的家兔模型,研究吸入一氧化氮对大面积肺血栓栓塞症家兔血心肌肌钙蛋白(CTnI)浓度的影响。方法日本大白兔30只,分为试验组10只,只对家兔进行大面积肺血栓栓塞症心肌受损的模型试验;对照组10只,常规溶栓治疗;治疗组10只,常规溶栓治疗合并吸入一氧化氮治疗,一氧化氮吸入浓度为40×10-6g/L,试验组、对照组、治疗组于模型制备成功后每4h抽血共48h,多道生理参数分析记录仪,同步检测动脉平均压和肺动脉平均压。结果家兔大面积肺栓塞后8h心肌肌钙蛋白(CTnI)全部阳性,其峰浓度出现所需时间(18.8±4.5)h,心肌肌钙蛋白阳性持续时间(38.6±5.2)h,其心肌肌钙蛋白峰浓度值为(0.42±0.12)μg/L,家兔心肌肌钙蛋白浓度与动脉平均压和肺动脉平均压均无相关性,心肌肌钙蛋白峰浓度与其同时间点的肺动脉平均压程明显的相关性(r=0.98,P<0.05)。其心肌肌钙蛋白峰浓度出现所需时间和阳性持续时间对照组较试验组明显缩短[(15.1±3.2)svs(18.8±4.5)s,P<0.048;(34.1±3.5)svs(38.6±5.2)s,P<0.036),治疗组较对照组亦明显缩短[(12.4±2.4)svs(15.1±3.2)s,P<0.047;(31.0±2.2)svs(34.1±3.5)s,P<0.03)],心肌肌钙蛋白峰浓度对照组较试验组明显降低[(0.31±0.10)μg/Lvs(0.42±0.12)μg/L,P<0.039),治疗组较对照组亦明显降低[(0.21±0.06)μg/Lvs(0.31±0.10)μg/L,P﹤0.014)]。对照组溶栓后肺动脉平均压变化曲线先有上升,达高峰后逐渐降低,治疗组肺动脉平均压变化曲线先有降低,随后上升,达高峰后逐渐降低,随机抽取对照组和治疗组两曲线上几个时间点的肺动脉平均压比较均有明显差异。结论吸入一氧化氮能明显降低肺动脉平均压和心肌肌钙蛋白峰浓度,对大面积肺血栓栓塞症家兔心肌受损有明显的保护作用。【Objective】To make cardiac muscle injure animals model of the rabbits with acute massive pulmonary embolism, investigate the effect of inhalation nitric oxide on cardiac troponin I and pulmonary arterial pressure of rabbits with acute massive pulmonary embolism. 【Methods】 30 Japanese white rabbits were randomly divided into the experimental group, contrast group , control group （conventional thrombolysis therapy by guideline of diagnosis and therapy of pulmonary embolism）, treatment group （conventional therapy and nitric oxide inhalation of 40×10-6 g/L）. Cardiac troponin I concentration and pulmonary arterial pressure was measured every 4 h for 48 h after animals models has successfully been finished. 【Results】 The cardiac troponin I of rabbits with acute massive pulmonary embolism became positive in within 8 h. After a median of （18.8 ± 4.5） h, cardiac troponin I peaked to a median of （0.42 ± 0.12） μg/L, cardiac troponin I persisted positive for a median of （38.6 ± 5.2） h, the relative was not in between rabbits arterial pressure and cardiac troponin I, and that between rabbits pulmonary arterial pressure and cardiac troponin I, but the relative was markedly in pulmonary arterial pressure and peak concentration of cardiac troponin I （r =0.98, P 0.05）, in control group： after thrombolysis pulmonary arterial pressure was raised firstly, then it reduced slowly after having peaked： in treatment group, it was reduced, then raised, afterwards it reduced slowly after having peaked, several points pulmonary arterial pressure was take out randomly in tow groups, they all have marked distant. The time of cardiac troponin I peak value occurred and cardiac troponin I persisted positive were obviously shorter in control group than that experimental group [（15.1 ± 3.2） s vs （18.8 ± 4.5） s,P﹤0.048;（34.1 ± 3.5） s vs （38.6 ± 5.2） s,P 0.036）], so were treatment group than that control group [（12.4 ± 2.4） s vs （15.1 ± 3.2） s,P﹤ 0.047;（31.0 ± 2.2）

关 键 词：肺血栓 家兔 治疗 吸入一氧化氮 肺动脉平均压 

分 类 号：R-332[医药卫生] R543.2