Chyczewski L, Debek W
Patol Pol. 1989;40(1):29-37.
Quantification of MK in blood and pulmonary sections was performed in rabbits with induced hemorrhagic shock (group I) and in control rabbits (group II). In electron transmission microscopy we studied the ultrastructure of pulmonary capillaries. Animals in group I were exsanguinated to achieve systemic blood pressure level of 40 mm Hg. This level was maintained for 1.5 hours and then the rabbits from both groups were sacrificed. Pulmonary arterial and venous blood was sampled in the amount of 10 ml and two sections from each pulmonary lobe were taken. The blood samples were then treated with Streptolysine 0 in order to isolate MK which were counted in the smears. In pulmonary sections MKs were counted per 1 cm2. In animals with shock we found an increase in MKs in the pulmonary artery (means = 4.9 MK/ml against means = 1 MK/ml in venous blood; corresponding values for group II were means = 1.7 MK/ml and 1 MK ml respectively). In the lungs of rabbits in group I we found considerable accumulation of MKs means = 22.4 MK/cm2 (corresponding value for group II means = 2 MK/cm2). It was found that hemorrhagic shock was probably the factor activating the release of MK from the bone marrow to the periferal blood, whereas pulmonary capillaries were an effective filter uptaking circulating MKs. Edematous changes in the capillary endothelium were probably the factors intensifying the process of pulmonary uptake of MK. We discussed the value of pulmonary accumulation of MK in the development of mechanisms leading to adult respiratory distress syndrome.
对诱导出血性休克的兔子(I组)和对照兔子(II组)的血液和肺部切片中的巨核细胞(MK)进行了定量分析。在电子透射显微镜下,我们研究了肺毛细血管的超微结构。I组动物放血以达到40 mmHg的全身血压水平。该水平维持1.5小时,然后处死两组兔子。采集10 ml肺动脉和静脉血,并从每个肺叶取两片组织切片。然后用链球菌溶血素O处理血样以分离巨核细胞,并在涂片上进行计数。在肺部切片中,每平方厘米计数巨核细胞数量。在休克动物中,我们发现肺动脉中的巨核细胞增加(平均值 = 4.9个巨核细胞/毫升,而静脉血中的平均值 = 1个巨核细胞/毫升;II组的相应值分别为平均值 = 1.7个巨核细胞/毫升和1个巨核细胞/毫升)。在I组兔子的肺中,我们发现巨核细胞大量积聚(平均值 = 22.4个巨核细胞/平方厘米,II组的相应值平均值 = 2个巨核细胞/平方厘米)。结果发现,出血性休克可能是促使巨核细胞从骨髓释放到外周血的因素,而肺毛细血管是摄取循环中巨核细胞的有效滤器。毛细血管内皮的水肿变化可能是加剧肺摄取巨核细胞过程的因素。我们讨论了肺中巨核细胞积聚在导致成人呼吸窘迫综合征机制发展中的价值。