家兔油酸中毒性肺水肿时肺血流动力学改变

The changes of pulmonary hemodynamics of pulmonary edema induced by oleic acid in rabbits

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。

It was an dideal model of respiratory distress syndyomeinduccd in 59 rabbits by Ⅳ oleic acid injection. Pulmonary hemodynamics, cardiac impedance paramcters were measured, microemboli and leukocytcs were abtained directly from the pulmonary microcirculation by use of the retrograde perfusion method. The results showed that pulmonary hemodynamics were changed significantly, but did not correlate with development of pulmonary edema. It was found that basic impedance (Zo) increased, stroke volume (SV), cardiac output (CO) and cardiac index (CI) all decreased (P<0.01). It was also found that a great number of microemboli and leukocytes (19.7×10~6/L and 2390×10~6/L, respectively) were deposited in the pulmonary microcirculation as compared with the control group (1×106/L, 430×10~6/L respectively, P<0.01). These findings indicate that changes of pulmonary hemodynamics are not primary pathogenic factors of pulmonary edema induced by oleic acid. Leukocytes sequestration in the pulmonary microcirculation is a pathologic reaction induced by oleic acid, the effect of micioemboIi on pulmonary damage is not clear yet.