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油酸诱导的肺损伤中的肺血管收缩。一项形态计量学研究。

Pulmonary vasoconstriction in oleic acid induced lung injury. A morphometric study.

作者信息

Grotjohan H P, van der Heijde R M, Wagenvoort C A, Wagenvoort N, Versprille A

机构信息

Department of Pulmonary Diseases, Erasmus University Rotterdam, The Netherlands.

出版信息

Int J Exp Pathol. 1993 Aug;74(4):347-55.

Abstract

Distribution and severity of active vasoconstriction of muscular pulmonary arteries were morphometrically assessed in anaesthetized, paralysed and mechanically ventilated pigs with respiratory distress, induced by oleic acid. Vasoconstriction was deduced from the medial thickness which was measured and expressed as a percentage of external diameter. Six pigs received oleic acid (0.12 +/- 0.07 ml/kg), dissolved 1:1 in 96% alcohol, in multiple injections of 0.1 ml. Six pigs were used as controls. After the oleic acid injections a stable hypoxaemia (PaO2 = 57 +/- 8 mmHg, at an inspiratory oxygen fraction of 0.6) and pulmonary hypertension (mean Ppa = 36 +/- 2 mmHg) were obtained for several hours. Electron microscopy revealed swelling of endothelial cells with signs of degeneration. Medial thickness was far greater in the oleic acid group than in the control group; overall mean values were 8.1 +/- 3.2 and 3.8 +/- 1.7% respectively (P < 0.001). Arteries with prominent vasoconstriction were lying in clusters. This pattern was the same in dependent and non-dependent regions. We concluded that in oleic acid induced respiratory distress active vasoconstriction of muscular pulmonary arteries is an important factor in the development of pulmonary hypertension. Besides vasoconstriction, endothelial swelling and intravascular clotting may contribute to the development of pulmonary hypertension.

摘要

在经油酸诱导产生呼吸窘迫的麻醉、麻痹并机械通气的猪身上,采用形态测量法评估了肌型肺动脉活性血管收缩的分布和严重程度。血管收缩通过测量中膜厚度得出,并表示为外径的百分比。6只猪接受溶解于96%乙醇(比例为1:1)的油酸(0.12±0.07 ml/kg),每次注射0.1 ml,分多次注射。6只猪作为对照。注射油酸后,在吸入氧分数为0.6的情况下,出现了持续数小时的稳定低氧血症(动脉血氧分压=57±8 mmHg)和肺动脉高压(平均肺动脉压=36±2 mmHg)。电子显微镜检查显示内皮细胞肿胀并有退变迹象。油酸组的中膜厚度远大于对照组;总体平均值分别为8.1±3.2%和3.8±1.7%(P<0.001)。有明显血管收缩的动脉成簇分布。在下垂区和非下垂区这种模式相同。我们得出结论,在油酸诱导的呼吸窘迫中,肌型肺动脉的活性血管收缩是肺动脉高压发生发展的一个重要因素。除血管收缩外,内皮肿胀和血管内凝血可能也有助于肺动脉高压的发展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1546/2001855/ecfcd3a5e8d0/ijexpath00016-0029-a.jpg

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