Schlag G, Voigt W H, Schnells G, Glatzl A
Anaesthesist. 1976 Nov;25(11):512-21.
The material investigated was obtained by lung puncture with the aid of the Hausser needle. The puncture technique as well as the preparation of the biopsy material for electronmicroscopic diagnostics are described. The most outstanding criterion in all biopsies examined is the large number of polymorphonuclear, mainly neutrophile granulocytes in the capillary and precapillary arterioles. In contrast, hardly any platelets were found in pulmonary vessels. Also, our investigation of the material revealed no intravascular fibrin deposits while vessels are partly and sometimes completely occluded by fat droplets of different size. The vascular walls are markedly swollen. Fluid escape from smaller vessels results in an edematous swelling of varying degree in the perivascular space combined with fibrin uptake and partly or totally destroyed cell structures. The type I epithelial cells of the lung tissue are swollen and show poor cellular structures. There is in increase of the type II epithelial cells in the shock lung with their lamellary corpuscles partly transferred into the alveolar lumen. The pathomechanisms leading to these changes are discussed. We would like to point out that fibrin was never found intravascularly but was always seen in regions. These findings could indicate increased fibrinolytic activity in shock. Platelet aggregations in smaller vessels are of secondary significance in the material we examined while fat globules, however, play an important part due to their large surface extension. Our electronmicroscopic investigations prove that the lung biopsy method is of great importance for further information on the pathologenesis of early damages in the shock lung not easily discovered by light microscopy.
所研究的材料是借助豪泽针通过肺穿刺获得的。文中描述了穿刺技术以及用于电子显微镜诊断的活检材料的制备方法。在所有检查的活检标本中,最显著的标准是在毛细血管和毛细血管前小动脉中有大量多形核细胞,主要是中性粒细胞。相比之下,在肺血管中几乎未发现血小板。此外,我们对材料的研究表明,血管内没有纤维蛋白沉积,而血管部分或有时完全被不同大小的脂肪滴阻塞。血管壁明显肿胀。较小血管的液体渗出导致血管周围间隙不同程度的水肿性肿胀,并伴有纤维蛋白摄取以及部分或完全破坏的细胞结构。肺组织的I型上皮细胞肿胀,细胞结构不佳。休克肺中II型上皮细胞增多,其板层小体部分转移到肺泡腔内。文中讨论了导致这些变化的病理机制。我们想指出的是,从未在血管内发现纤维蛋白,而是总是在某些区域看到。这些发现可能表明休克时纤维蛋白溶解活性增加。在我们检查的材料中,较小血管中的血小板聚集具有次要意义,而脂肪球由于其大的表面积扩展则起着重要作用。我们的电子显微镜研究证明,肺活检方法对于进一步了解休克肺早期损伤的病理发生机制非常重要,而这些损伤通过光学显微镜不易发现。