Gardner David S, Giussani Dino A
Department of Physiology, University of Cambridge, Downing St, Cambridge, CB2 3EG, UK.
Circulation. 2003 Jul 22;108(3):331-5. doi: 10.1161/01.CIR.0000080323.40820.A1. Epub 2003 Jun 30.
The continuing incidence of intrapartum morbidity may be partly due to antenatal compromise, which influences the fetal defense to labor and delivery. We have shown that antenatal exposure of the ovine fetus to partial compression of the umbilical cord suppresses femoral vasoconstriction during subsequent acute hypoxemia through elevated nitric oxide (NO) activity. This study investigated whether elevated NO activity in cord-compressed fetuses enhanced the vasodilator response to hypoxemia in circulations in which blood flow is known to increase during acute hypoxemia, such as the umbilical vascular bed.
Fifteen fetal sheep were chronically instrumented between 117 and 120 days of gestation with vascular catheters and an umbilical flow probe. In 8 of these fetuses, umbilical blood flow was reduced by 30% for 3 days between 125 and 128 days. The remaining 7 fetuses acted as sham-operated controls. Between 2 and 7 days after umbilical cord/sham compression, fetuses were exposed to 2 episodes of acute hypoxemia, on separate days, during infusion with either saline or treatment with a combination of NG-nitro-l-arginine methyl ester and sodium nitroprusside. The data show that umbilical cord compression significantly enhances the umbilical hyperemia through NO-dependent mechanisms during a subsequent episode of acute hypoxemia.
Increased fetal NO activity after chronic cord compression has opposing effects in circulations that either constrict or dilate during subsequent acute hypoxemia. The data imply that antenatal compromise switches the fetal strategy to withstand episodes of subsequent acute hypoxemia of the type that may occur during labor and delivery from a reliance on vasoconstrictor mechanisms to those promoting NO-dependent vasodilation.
产时发病的持续发生可能部分归因于产前的损害，这会影响胎儿对分娩的防御能力。我们已经表明，产前羊胎儿暴露于脐带部分受压会通过升高一氧化氮（NO）活性来抑制随后急性低氧血症期间的股动脉血管收缩。本研究调查了脐带受压胎儿中升高的NO活性是否增强了在急性低氧血症期间已知血流量会增加的循环系统（如脐血管床）中对低氧血症的血管舒张反应。
15只妊娠117至120天的胎羊通过血管导管和脐血流探头进行长期仪器植入。其中8只胎羊在妊娠125至128天期间，脐带血流减少30%，持续3天。其余7只胎羊作为假手术对照。在脐带/假手术受压后2至7天，胎羊在分别的日子里接受2次急性低氧血症发作，期间输注生理盐水或用NG-硝基-L-精氨酸甲酯和硝普钠联合治疗。数据表明，在随后的急性低氧血症发作期间，脐带受压通过依赖NO的机制显著增强了脐部充血。
慢性脐带受压后胎儿NO活性增加在随后急性低氧血症期间收缩或舒张的循环系统中具有相反的作用。数据表明，产前损害将胎儿抵御分娩期间可能发生的后续急性低氧血症发作的策略从依赖血管收缩机制转变为促进依赖NO的血管舒张机制。
