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用创伤性和非创伤性方法监测家兔肺血液动力学及心功能的改变,用肺循环逆流灌洗法对肺微循环中微栓及白细胞进行计数。结果显示油酸性肺水肿时平均肺动脉压及肺血管阻力分别升高49%和464%;平均肺血流量下降42%。心阻抗参数与注油酸前比Zo明显增加,SV,CO,CI都有明显下降(P<0.01)。肺微循环逆流灌洗液中微栓和白细胞比对照组明显增加(P<0.01)。肺重量增加1倍,但水肿液中水份所占比例(90.6%)与血浆中水份(91.5%)相接近。提示油酸性肺水肿时肺血液动力学改变显著,但不是肺水肿发病的根本因素;油酸性肺水肿时存在心功能减弱,机制有待于研究;白细胞在肺中滞留是油酸引起的病理反应,但非原发性病因学因素,微栓对肺损伤的作用尚不明确。
Pulmonary hemodynamics and changes in cardiac function were monitored by traumatic and non-invasive methods. Pulmonary circulation counter-current lavage was used to count microthrombi and leukocytes in the pulmonary microcirculation. The results showed that the mean pulmonary artery pressure and pulmonary vascular resistance were increased by 49% and 466%, respectively, in the acid-acid pulmonary edema; the mean pulmonary blood flow decreased by 42%. The cardiac impedance parameters and oleic acid significantly increased before Zo, and SV, CO, and CI decreased significantly (P<0.01). Pulmonary microcirculation countercurrent lavage fluid in the micro-thrombus and white blood cells than the control group increased significantly (P <0.01). The weight of the lungs increased by a factor of 2, but the proportion of water in the edema fluid (90.6%) was similar to that of plasma (91.5%). It suggested that the pulmonary hemodynamic changes were significant in acidotic pulmonary edema, but it was not a fundamental factor in the pathogenesis of pulmonary edema; there was a weakened heart function in oleic acid pulmonary edema, and the mechanism remained to be studied; leukocyte retention in the lung was a pathological reaction caused by oleic acid. However, non-primary etiological factors, the role of microbolus on lung injury is not yet clear.