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首页> 外文期刊>American Journal of Physiology >Factors that increase the contractile tone of the ductus arteriosus also regulate its anatomic remodeling.
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Factors that increase the contractile tone of the ductus arteriosus also regulate its anatomic remodeling.

机译：增加动脉导管收缩张力的因素也调节其解剖重塑。

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Permanent closure of the full-term newborn ductus arteriosus (DA) occurs only if profound hypoxia develops within the vessel wall during luminal obliteration. We used fetal and newborn baboons and lambs to determine why the immature DA fails to remodel after birth. When preterm newborns were kept in a normoxic range (Pa(O(2)): 50-90 mmHg), 86% still had a small patent DA on the sixth day after birth; in addition, the preterm DA wall was only mildly hypoxic and had only minimal remodeling. The postnatal increase in Pa(O(2)) normally induces isometric contractile responses in rings of DA; however, the excessive inhibitory effects of endogenous prostaglandins and nitric oxide, coupled with a weaker intrinsic DA tone, make the preterm DA appear to have a smaller increment in tension in response to oxygen than the DA near term. We found that oxygen concentrations, beyond the normoxic range, produce an additional increase in tension in the preterm DA that is similar to the contractile response normally seen at term. We predicted that preterm newborns, kept at a higher Pa(O(2)), would have increased DA tone and would be more likely to obliterate their lumen. We found that preterm newborns, maintained at a Pa(O(2)) >200 mmHg, had only a 14% incidence of patent DA. Even though DA constriction was due to elevated Pa(O(2)), obliteration of the lumen produced profound hypoxia of the DA wall and the same features of remodeling that were observed at term. DA wall hypoxia appears to be both necessary and sufficient to produce anatomic remodeling in preterm newborns.
机译：仅当管腔闭塞过程中血管壁内出现严重的缺氧时，才会永久关闭足月新生儿动脉导管（DA）。我们使用胎儿和新生的狒狒和羔羊来确定为什么未成熟的DA在出生后无法重塑。当早产儿保持在常氧范围内（Pa（O（2））：50-90 mmHg）时，有86％的人在出生后第六天仍有少量DA。此外，早产DA壁仅轻度缺氧，并且仅具有最小程度的重塑。产后Pa（O（2））的增加通常会在DA的环中引起等距的收缩反应。然而，内源性前列腺素和一氧化氮的过度抑制作用，再加上较弱的内在DA音调，使得早产DA对氧的张力似乎比近期DA的张力增量小。我们发现，氧浓度超出常氧范围，会使早产DA的张力进一步增加，这与足月正常情况下的收缩反应相似。我们预测，保持较高Pa（O（2））的早产儿会增加DA音调，并且更有可能消除其管腔。我们发现，维持Pa（O（2））> 200 mmHg的早产儿，发生专利性DA的发生率仅为14％。即使DA收缩是由于Pa（O（2））升高引起的，管腔的闭塞也导致DA壁严重缺氧，并具有足月观察到的重塑特征。 DA壁缺氧似乎对于早产儿产生解剖学重构既必要又充分。

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