Ivey Kathryn N, Srivastava Deepak
Gladstone Institute of Cardiovascular Disease, University of California San Francisco, San Francisco, California 94158, USA.
J Clin Invest. 2006 Nov;116(11):2863-5. doi: 10.1172/JCI30349.
The ductus arteriosus (DA) is a vessel whose patency is required for fetal survival but is incompatible with postnatal life. Because of developmental insufficiency, the DA in preterm infants often fails to close in a condition known as patent DA (PDA). Although COX inhibitors can be used to close the PDA by lowering circulating prostaglandin levels, their effectiveness is correlated with birth weight, and severely premature infants often require surgical repair. Paradoxically, targeted deletion of COX pathway components in mice results in PDA. In this issue of the JCI, Yokoyama et al. describe dual roles for prostaglandins in DA development and closure, offering new insights into the mechanism of negative effects of COX inhibitors that may influence the treatment of severely premature infants with PDA and lead to improvement of their outcomes (see the related article beginning on page 3026).
动脉导管(DA)是一种胎儿存活所必需保持通畅但与出生后生命不相容的血管。由于发育不全,早产儿的动脉导管常常在一种称为动脉导管未闭(PDA)的情况下无法闭合。尽管环氧化酶(COX)抑制剂可通过降低循环前列腺素水平来闭合动脉导管未闭,但它们的有效性与出生体重相关,而且极早产儿通常需要手术修复。矛盾的是,在小鼠中靶向删除COX途径成分会导致动脉导管未闭。在本期《临床研究杂志》中,横山等人描述了前列腺素在动脉导管发育和闭合中的双重作用,为COX抑制剂负面影响的机制提供了新见解,这可能会影响对患有动脉导管未闭的极早产儿的治疗并改善其预后(见第3026页开始的相关文章)。