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目的:采用人工血管肺动脉-左心房分流与肺动脉环缩的方法建立慢性肺血减少性发绀幼猪模型。方法:6～8周龄幼猪分为2组,模型组7只先行人工血管肺动脉-左心房分流后环缩主肺动脉,对照组6只仅开胸。饲养4周后行2次手术,测量肺动脉环缩处压差及动脉血气分析。结果:对照组均存活,模型组存活6只。模型组建模4周后与建立初比较,动脉血氧饱和度、pa(O2)和pH明显降低(P<0.05),而血红蛋白、血细胞比容和pa(CO2)均明显升高(P<0.01)。肺动脉环缩处的压差由(1.37±0.81)kPa增至4周后的(2.62±0.63)kPa(P<0.05)。4周后模型组的动脉血氧饱和度、pa(O2)、pa(CO2)、血红蛋白和血细胞比容与对照组比较差异均有统计学意义(P<0.05)。结论:应用人工血管肺动脉-左心房分流与肺动脉环缩的方法成功建立慢性肺血减少性发绀动物模型,该模型创伤小、可重复性高,为发绀型肺血减少先天性心脏病的基础及临床研究提供可靠的模型平台和理论依据。
OBJECTIVE: To establish a model of cyanosis-deficient cyanosis piglets by artificial pulmonary artery-left atrium shunt and pulmonary artery systole. Methods: Six to eight-week-old young pigs were divided into two groups. Seven rabbits in the model group received artificial pulmonary artery-to-left atrial shunts and the main pulmonary arteries were shunted. Six of the control group received thoracotomy only. After 4 weeks of rearing, 2 surgeries were performed to measure the pulmonary systolic pressure drop and arterial blood gas analysis. Results: The control group survived, the model group survived 6. At 4 weeks after model establishment, arterial oxygen saturation, pa (O2) and pH were significantly decreased (P <0.05), and hemoglobin, hematocrit and pa (CO2) 0.01). The pressure drop of pulmonary artery systole was increased from (1.37 ± 0.81) kPa to (2.62 ± 0.63) kPa after 4 weeks (P <0.05). After 4 weeks, the arterial oxygen saturation, pa (O2), pa (CO2), hemoglobin and hematocrit in the model group were significantly different from those in the control group (P <0.05). CONCLUSIONS: Chronic pulmonary hypoperfusion cyanosis animal model was successfully established by artificial pulmonary artery-left atrium shunt and pulmonary artery systole. This model has the advantages of less trauma and high reproducibility, and is the basis of reducing cyanotic pulmonary blood flow in congenital heart disease Clinical research provides a reliable model platform and theoretical basis.