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对蛋白是否抑制肺表面活性物质（ＳＡＭ）活性，进行了大白鼠体内外实验。体外实验，测定了不同浓度的血浆蛋白和ＳＡＭ混和液标本的最小表面张力（ＳＴｍｉｎ）和最大表面张力（ＳＴｍａｘ）；体内实验，将大白鼠随机分为血浆组、生理盐水组和对照组，分别向前两组动物肺内注入血浆或生理盐水。结果发现，体外实验随蛋白浓度的增高，ＳＴｍｉｎ和ＳＴｍａｘ也增高，呈现浓度依赖关系；体内实验血浆组和盐水组大鼠空气机械通气３０分钟后ＰＯ２和顺应性明显低于对照组，继续纯氧通气１０分钟，两组动物ＰＯ２仍明显低于对照组，而血浆组ＰＯ２又明显低于盐水组。作者认为，盐水组ＰＯ２下降主要与生理盐水稀释ＳＡＭ有关，血浆组ＰＯ２下降主要是血浆蛋白抑制了ＳＡＭ活性，使其功能不良
Whether the protein inhibits the activity of pulmonary surfactant (SAM), in vivo experiments in rats were performed. In vitro experiments, the minimum surface tension (STmin) and maximum surface tension (STmax) of different concentrations of plasma protein and SAM mixture were measured; in vivo experiments, the rats were randomly divided into plasma group, saline group and control group Two groups of animals were injected with plasma or saline into their lungs. The results showed that in vitro experiments with increasing protein concentration, STmin and STmax also increased in a concentration-dependent manner; in vivo experimental plasma and saline rats air mechanical ventilation 30 minutes after PO2 and compliance was significantly lower than the control group continued pure oxygen Ventilation for 10 minutes, PO2 in both groups was still significantly lower than the control group, while plasma PO2 was significantly lower than saline group. The authors believe that the decrease of PO2 in saline group was mainly related to the dilution of SAM by saline, the decrease of PO2 in plasma was mainly due to inhibition of SAM activity by plasma protein and dysfunction