Sheehan P M, Stokes D C, Yeh Y Y, Hughes W T
Am Rev Respir Dis. 1986 Sep;134(3):526-31. doi: 10.1164/arrd.1986.134.3.526.
The effect of Pneumocystis carinii pneumonia on surfactant phospholipids and lavage phospholipase A2 was investigated. Pneumocystis carinii infection was induced in adult rats by immunosuppression with dexamethasone administered in the drinking water (2 mg/L) for 6 to 8 wk. Surfactant phospholipids were isolated from lung lavage and lung tissue. Dexamethasone administration significantly increased total lung and lavage phospholipids in corticosteroid-treated animals receiving prophylaxis against P. carinii with trimethoprim-sulfamethoxazole (TMP-SMZ) when compared with no treatment control animals. Lavage surfactant phospholipids from P. carinii-infected rats were 25% that of no treatment control rats and less than 10% that of corticosteroid control animals receiving TMP-SMZ. Phospholipid composition of lavage phospholipids was also altered in P. carinii pneumonia, with slight increase in the percentage of sphingomyelin and reduced percentage of total phosphatidylcholine. Postlavage tissue phospholipids of P. carinii-infected rats were 4 times that of no treatment control animals, although only about 50% that of corticosteroid control animals. There was no significant difference in lavage phospholipase A2 activity for the P. carinii-infected and corticosteroid control groups, although the enzyme activity was at least 4 times that of the no treatment control group. The surfactant changes were associated with abnormal excised lung pressure-volume curves and decreased deflation stability in the animals with P. carinii. These results indicate that the corticosteroids used in this model induce an increase in both lung surfactant phospholipids and phospholipase A2. Despite this increase in lavage phospholipids, P. carinii pneumonia in this model causes an alveolar surfactant phospholipid deficiency without significant increase in phospholipase A2 activity.(ABSTRACT TRUNCATED AT 250 WORDS)
研究了卡氏肺孢子虫肺炎对表面活性物质磷脂和灌洗磷脂酶A2的影响。通过在饮用水中给予地塞米松（2mg/L）进行免疫抑制6至8周，在成年大鼠中诱导卡氏肺孢子虫感染。从肺灌洗物和肺组织中分离表面活性物质磷脂。与未治疗的对照动物相比，在接受甲氧苄啶 - 磺胺甲恶唑（TMP - SMZ）预防卡氏肺孢子虫的皮质类固醇治疗动物中，给予地塞米松显著增加了总肺和灌洗磷脂。卡氏肺孢子虫感染大鼠的灌洗表面活性物质磷脂是未治疗对照大鼠的25%，不到接受TMP - SMZ的皮质类固醇对照动物的10%。卡氏肺孢子虫肺炎中灌洗磷脂的磷脂组成也发生了改变，鞘磷脂百分比略有增加，总磷脂酰胆碱百分比降低。卡氏肺孢子虫感染大鼠灌洗后组织磷脂是未治疗对照动物的4倍，尽管仅约为皮质类固醇对照动物的50%。卡氏肺孢子虫感染组和皮质类固醇对照组的灌洗磷脂酶A2活性没有显著差异，尽管该酶活性至少是未治疗对照组的4倍。表面活性物质的变化与卡氏肺孢子虫感染动物异常的离体肺压力 - 容积曲线和放气稳定性降低有关。这些结果表明，该模型中使用的皮质类固醇会导致肺表面活性物质磷脂和磷脂酶A2均增加。尽管灌洗磷脂增加，但该模型中的卡氏肺孢子虫肺炎导致肺泡表面活性物质磷脂缺乏，而磷脂酶A2活性没有显著增加。（摘要截短至250字）
