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胎粪吸入综合征:磷脂酶A2在发病机制中的作用?

Meconium aspiration syndrome: a role for phospholipase A2 in the pathogenesis?

作者信息

Kääpä P

机构信息

Research Center of Applied and Preventive Cardiovascular Medicine and Department of Pediatrics, University of Turku, Finland.

出版信息

Acta Paediatr. 2001 Apr;90(4):365-7.

Abstract

UNLABELLED

The pathophysiology of neonatal meconium aspiration syndrome (MAS), often resulting in severe respiratory failure, is complex and still largely unclear. Factors involved in the propagation of acute lung injury after perinatal aspiration of meconium include obstruction of the airways, ventilation/perfusion mismatch, increase of the pulmonary vascular resistance and a rapidly developing parenchymal and alveolar inflammatory reaction with associated surfactant dysfunction.

CONCLUSION

Although the early pulmonary inflammatory response is believed to play a central pathogenetic role in the meconium-induced acute lung damage, its initiating mechanisms are still poorly defined. However, increasing evidence indicates a direct toxic effect of meconium.

摘要

未标注

新生儿胎粪吸入综合征(MAS)的病理生理学机制复杂,目前仍不清楚,该综合征常导致严重呼吸衰竭。围产期吸入胎粪后急性肺损伤进展过程中涉及的因素包括气道阻塞、通气/血流不匹配、肺血管阻力增加以及实质和肺泡迅速发生的炎症反应并伴有表面活性物质功能障碍。

结论

尽管早期肺部炎症反应被认为在胎粪诱导的急性肺损伤中起核心致病作用,但其启动机制仍不明确。然而,越来越多的证据表明胎粪具有直接毒性作用。

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