Robertson B
Research Unit for Experimental Perinatal Pathology, St. Göran's Hospital, Stockholm, Sweden.
Dev Pharmacol Ther. 1989;13(2-4):159-63. doi: 10.1159/000457599.
The neonatal respiratory distress syndrome (RDS), caused by surfactant deficiency, is characterized by a nonuniform distribution of tidal volumes in the lung parenchyma, epithelial necrosis in peripheral airspaces, and leakage of protein into the alveoli from areas of epithelial disruption. Studies on premature experimental animals have shown that the leakage of protein is correlated to the pressure required to ventilate the lungs, i.e. presumably to the degree of surfactant deficiency. Since the leaking material includes potent surfactant inhibitors, the underlying surfactant deficiency may become aggravated, and a vicious cycle is easily established. Lung compliance is improved, epithelial necrosis prevented, and protein leakage significantly reduced by instillation of surfactant into the airways of immature newborn experimental animals. This provides the rationale for surfactant replacement therapy in neonatal RDS.
新生儿呼吸窘迫综合征(RDS)由表面活性物质缺乏引起,其特征为肺实质内潮气量分布不均、外周气腔上皮坏死以及蛋白质从上皮破坏区域漏入肺泡。对早产实验动物的研究表明,蛋白质渗漏与肺通气所需压力相关,即可能与表面活性物质缺乏程度相关。由于渗漏物质包括强效表面活性物质抑制剂,潜在的表面活性物质缺乏可能会加重,从而容易形成恶性循环。通过向未成熟新生实验动物气道内滴注表面活性物质,可改善肺顺应性、预防上皮坏死并显著减少蛋白质渗漏。这为新生儿RDS的表面活性物质替代疗法提供了理论依据。