Department of Biological Sciences, Developmental Integrative Biology Cluster, University of North Texas, Denton, TX, USA; Zoophysiology, Department of Bioscience, Aarhus University, Aarhus, Denmark.
Acta Physiol (Oxf). 2014 Jun;211(2):346-57. doi: 10.1111/apha.12286. Epub 2014 Apr 18.
Prenatal hypoxia due to placental insufficiency results in deleterious phenotypes and compensatory mechanisms including increased sympathetic tone. Utilizing the embryonic chicken model, we investigated (i) changes in nitric oxide (NO)-mediated tone in response to chronic hypoxic development and (ii) the in vivo role of NO-mediated tone during acute hypoxic exposure, which has not been previously studied. We hypothesized that NO tone on the cardiovascular system would be unaffected by chronic hypoxic incubation in White Leghorn chicken (Gallus domesticus) embryos.
We measured arterial pressure, heart rate and femoral blood flow (via a Doppler flow probe) in response to acute hypoxia (10% O2 ) and pharmacological manipulations in normoxic- and hypoxic (15% O2 )-incubated embryos. This was performed at 70 and 90% of total incubation time (21 days). At 70% of incubation (day 15), blood volume and chorioallantoic membrane development are maximal; 90% of incubation (day 19) is 1 day prior to lung ventilation.
Acute hypoxic exposure decreased femoral flow in both 90% groups, but increased femoral artery resistance in the hypoxic group. NO tone increased during development, but was not affected by hypoxic incubation. Inhibition of NO production by L-NAME (100 mg kg(-1) ) revealed that NO plays a significant role in the flow response to hypoxia.
Chronic hypoxic incubation has no effect on cardiovascular NO tone during White Leghorn chicken development. In the intact animal, NO function during acute hypoxic stress is suppressed by hypoxic incubation, indicating that chronic hypoxic stress dampens the NO contribution.
胎盘功能不全导致的产前缺氧会导致有害表型和代偿机制，包括增加交感神经张力。利用胚胎鸡模型，我们研究了（i）慢性缺氧发育过程中一氧化氮（NO）介导的张力变化，以及（ii）NO 介导的张力在急性缺氧暴露中的体内作用，这一点以前尚未研究过。我们假设，在白来亨鸡（Gallus domesticus）胚胎中，慢性低氧孵育不会影响心血管系统的 NO 张力。
我们在正常氧和低氧（15% O2）孵育的胚胎中测量了动脉血压、心率和股动脉血流（通过多普勒血流探头）对急性缺氧（10% O2）和药理学处理的反应。这是在总孵育时间的 70%和 90%（21 天）进行的。在孵育的 70%（第 15 天）时，血容量和绒膜尿囊膜发育达到最大值；孵育的 90%（第 19 天）是在肺通气前一天。
急性低氧暴露降低了 90%组的股动脉血流，但增加了低氧组的股动脉阻力。NO 张力在发育过程中增加，但不受低氧孵育的影响。NO 产生的抑制作用通过 L-NAME（100mg/kg(-1)）表明，NO 在血流对缺氧的反应中起着重要作用。
在白来亨鸡发育过程中，慢性低氧孵育对心血管 NO 张力没有影响。在完整的动物中，急性低氧应激期间的 NO 功能被低氧孵育抑制，表明慢性低氧应激抑制了 NO 的贡献。
