Schraufnagel D E, Schmid A
Department of Medicine, University of Illinois, Chicago 60680.
Am Rev Respir Dis. 1989 Nov;140(5):1405-9. doi: 10.1164/ajrccm/140.5.1405.
A mechanism for monocrotaline-induced pulmonary hypertension in experimental animals may be the loss of small blood vessels, but when pulmonary arteries have been studied, the results have been controversial. In this report, the density of the entire lung microvasculature as measured by gray-scale analysis of scanning electron microscopic images of corrosion casts is reported. In the first experiment, monocrotaline, 60 mg/kg, was injected intraperitoneally into Sprague-Dawley rats. After 16 days, the pulmonary vascular tree was cast with methylmethacrylate. The vascular density index of the casts at a magnification x 100 on the alveolar surface was 0.40 for the monocrotaline-treated animals and 0.48 for the saline-treated control animals (p less than 0.01). On the pleural surface, it was 0.51 for the monocrotaline animals and 0.67 for the saline animals (p less than 0.001). A second experiment found no significant difference in vascular density index between different doses of monocrotaline. Light and scanning electron microscopy suggest that capillary and small vessel thrombosis may account for the decrease in the density of vessels in pulmonary microvascular casts that occurs in response to monocrotaline.
实验动物中野百合碱诱导肺动脉高压的机制可能是小血管的丧失,但在对肺动脉进行研究时,结果存在争议。在本报告中,我们报告了通过对铸型扫描电子显微镜图像进行灰度分析测量的整个肺微血管系统的密度。在第一个实验中,将60mg/kg的野百合碱腹腔注射到Sprague-Dawley大鼠体内。16天后,用甲基丙烯酸甲酯对肺血管树进行铸型。在肺泡表面放大100倍时,野百合碱处理组动物铸型的血管密度指数为0.40,生理盐水处理对照组动物为0.48(p<0.01)。在胸膜表面,野百合碱组动物为0.51,生理盐水组动物为0.67(p<0.001)。第二个实验发现不同剂量野百合碱之间的血管密度指数无显著差异。光镜和扫描电镜显示,毛细血管和小血管血栓形成可能是野百合碱诱导肺微血管铸型中血管密度降低的原因。