Pentoxifylline reduces fibrin deposition and prolongs survival in neonatal hyperoxic lung injury.
Pentoxifylline reduces fibrin deposition and prolongs survival in neonatal hyperoxic lung injury.
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己酮可可碱可减少新生儿高氧性肺损伤的纤维蛋白沉积并延长生存期。
DOI:
10.1152/japplphysiol.00452.2004
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发表时间:
2004
期刊:
影响因子:
--
通讯作者:
Walther,FransJ
中科院分区:
文献类型:
--
作者:
terHorst,SimoneAJ;Wagenaar,GerryTM;deBoer,Eveline;vanGastelen,MargôtA;Meijers,JoostCM;Biemond,BartJ;Poorthuis,BenJHM;Walther,FransJ
Bronchopulmonary dysplasia is a leading cause of mortality and morbidity in preterm infants despite improved treatment modalities. Pentoxifylline, a phosphodiesterase inhibitor, inhibits multiple processes that lead to neonatal hyperoxic lung injury, including inflammation, coagulation, and edema. Using a preterm rat model, we investigated the effects of pentoxifylline on hyperoxia-induced lung injury and survival. Preterm rat pups were exposed to 100% oxygen and injected subcutaneously with 0.9% saline or 75 mg/kg pentoxifylline twice a day. Onday 10, lung tissue was harvested for histology, fibrin deposition, and mRNA expression, and bronchoalveolar lavage fluid was collected for total protein concentration. Pentoxifylline treatment increased mean survival by 3 days (P= 0.0018) and reduced fibrin deposition by 66% (P< 0.001) in lung homogenates compared with untreated hyperoxia-exposed controls. Monocyte chemoattractant protein-1 expression in lung homogenates was decreased, but the expressions of TNF-α, IL-6, matrix metalloproteinase-12, tissue factor, and plasminogen activator inhibitor-1 were similar in both groups. Total protein concentration in bronchoalveolar lavage fluid was decreased by 33% (P= 0.029) in the pentoxifylline group. Pentoxifylline treatment attenuates alveolar fibrin deposition and prolongs survival in preterm rat pups with neonatal hyperoxic lung injury, probably by reducing capillary-alveolar protein leakage.
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