Welsh D A, Guery B P, Deboisblanc B P, Dobard E P, Creusy C, Mercante D, Nelson S, Summer W R, Mason C M
Department of Medicine, Louisiana State University Medical Center, New Orleans, Louisiana 70112, USA.
Am J Physiol Heart Circ Physiol. 2001 Mar;280(3):H1311-7. doi: 10.1152/ajpheart.2001.280.3.H1311.
Hydrostatic pulmonary edema is a common complication of congestive heart failure, resulting in substantial morbidity and mortality. Keratinocyte growth factor (KGF) is a mitogen for type II alveolar epithelial and microvascular cells. We utilized the isolated perfused rat lung model to produce hydrostatic pulmonary edema by varying the left atrial and pulmonary capillary pressure. Pretreatment with KGF attenuated hydrostatic edema formation. This was demonstrated by lower wet-to-dry lung weight ratios, histological evidence of less alveolar edema formation, and reduced alveolar accumulation of intravascularly administered FITC-labeled large-molecular-weight dextran in rats pretreated with KGF. Thus KGF attenuates injury in this ex vivo model of hydrostatic pulmonary edema via mechanisms that prevent increases in alveolar-capillary permeability.
静水压性肺水肿是充血性心力衰竭的常见并发症，会导致严重的发病率和死亡率。角质形成细胞生长因子（KGF）是II型肺泡上皮细胞和微血管细胞的促分裂原。我们利用离体灌注大鼠肺模型，通过改变左心房和肺毛细血管压力来产生静水压性肺水肿。用KGF预处理可减轻静水压性水肿的形成。这在接受KGF预处理的大鼠中表现为较低的肺湿重与干重比值、肺泡水肿形成较少的组织学证据，以及血管内注射的异硫氰酸荧光素标记的大分子右旋糖酐在肺泡内的积聚减少。因此，KGF通过防止肺泡-毛细血管通透性增加的机制减轻了这种静水压性肺水肿离体模型中的损伤。
