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急性肺血栓栓塞症猪血流动力学及心肌损伤的研究
引用本文:Yang HS,Pan WS,Zhang LT,Guan JT,Ma JY,Ma N,Fu XH. 急性肺血栓栓塞症猪血流动力学及心肌损伤的研究[J]. 中华内科杂志, 2004, 43(9): 661-664
作者姓名:Yang HS  Pan WS  Zhang LT  Guan JT  Ma JY  Ma N  Fu XH
作者单位:1. 050000,石家庄,河北医科大学第二医院呼吸科
2. 050000,石家庄,河北医科大学第二医院心内科
摘    要:目的 观察急性肺血栓栓塞症 (PTE)猪血流动力学、动静脉血气及心肌肌钙蛋白Ⅰ(cTnⅠ )、肌红蛋白 (Mb)、肌酸激酶同工酶 (CK MB)水平。方法 健康幼年猪 16只 ,分为 2组 ,每组8只。栓塞组 (急性PTE模型组 ) :用注射器经颈外静脉插管快速 1次注入多聚乙烯微球 ,0 1g/kg体重悬浮于生理盐水 5 0ml中 ;对照组 :用注射器经颈外静脉插管快速 1次注入生理盐水 5 0ml。检测栓塞前、栓塞后即刻、30min、1h、2h、3h血流动力学及血气的变化 ,同时检测血清cTnⅠ、Mb、CK MB水平。结果 栓塞即刻肺动脉压升高 ,约为栓塞前的 2~ 3倍 ,栓塞后 2~ 3h逐渐恢复至栓塞前水平 ;心输出量、肺毛细血管嵌顿压、肺动脉压收缩压、舒张压无明显变化。栓塞即刻动脉血氧分压(PaO2 )下降 ,动脉血二氧化碳分压升高 ,pH值下降 ,30~ 6 0min达最高峰 ,2h后PaO2 和 pH值恢复至栓塞前水平。栓塞后血清cTnⅠ和Mb明显升高 ,CK Mb栓塞前后无明显变化。cTnⅠ与Mb有相关性 (r =0 5 5 ,P =0 0 0 1) ,与CK MB无相关性 (r =0 10 9,P =0 5 33)。结论 急性PTE可出现急性肺动脉压升高和气体交换障碍等病理生理改变。检测cTnⅠ和Mb有助于急性PTE心肌损伤早期诊断

关 键 词:急性肺血栓栓塞症 cTnⅠ PTE 升高 血流动力学 CK-MB 肺动脉压 水平 目的观 结论

Study on hemodynamic changes and cardiac troponin I level in pig model of acute experimental pulmonary embolism
Yang Hong-shen,Pan Wen-sen,Zhang Lu-tao,Guan Ji-tao,Ma Jun-yi,Ma Ning,Fu Xiang-hua. Study on hemodynamic changes and cardiac troponin I level in pig model of acute experimental pulmonary embolism[J]. Chinese journal of internal medicine, 2004, 43(9): 661-664
Authors:Yang Hong-shen  Pan Wen-sen  Zhang Lu-tao  Guan Ji-tao  Ma Jun-yi  Ma Ning  Fu Xiang-hua
Affiliation:Respiratory Department, the Second Hospital of Hebei Medical University, Shijiazhuang 050000, China.
Abstract:OBJECTIVE: To evaluate the hemodynamic effects and cardiac troponin I (cTn I), creatine kinase-MB (CK-MB), myoglobin (Mb) releasing kinetics of acute experimental pulmonary embolism of pigs. METHODS: Sixteen juvenile pigs, of either gender and weighing 30 to 40 kg were studied, 8 in the embolism group and 8 in the control group. The 8 embolism animals received 0.1 g/kg polystyrene beads (diameter range 0.65 to 0.67 mm) suspended in 0.9% saline by venous injection. Pulmonary arterial pressure (PAP), systemic arterial pressure (SAP), pulmonary capillary wedged pressure (PCWP), cardiac output (CO), blood gases and serum cTn I, CK-MB, and Mb were measured before and immediately, 30 min, 1 hour, 2 hour, and 3 hour after acute pulmonary embolism. RESULTS: PAP was increased to 2 - 3 fold of the baseline and the control level immediately, and then decreased to the baseline level in 2 to 3 hours. Serum cTn I and Mb increased significantly after embolism and remained at a higher level through the 3 hour experimental procedure. The CK-MB was not changed after acute pulmonary embolism. CONCLUSIONS: Acute pulmonary embolism caused lung gas exchange abnormality and acute pulmonary hypertension. The hemodynamic effects of acute pulmonary embolism include injury to the myocardial cells and releasing of cTn I and Mb to blood stream. cTn I can be detected in the early phase of acute pulmonary embolism, and maybe a useful marker in diagnosis and management of acute pulmonary embolism.
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