Hypoxic level and duration differentially affect embryonic organ system development of the chicken (Gallus gallus)
Hypoxic level and duration differentially affect embryonic organ system development of the chicken (Gallus gallus)
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DOI：
10.3382/ps.2012-02449
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发表时间：
2012-12-01
期刊：
影响因子：
4.4
通讯作者：
Burggren, W. W.
中科院分区：
文献类型：
--
作者：
Zhang, H.;Burggren, W. W.
缺氧抑制鸟类胚胎发育，并增加胚胎死亡率。然而，受缺氧影响的关键器官系统及其发育的关键窗口却知之甚少。因此，鸡胚连续暴露于3个水平的氧气（21，15，或13%的O-2）在整个d 0至10，d 11至18，或d 0至18的孵化，然后进行形态和血液生理测量。缺氧发生在孵化早期（D 0至10）有较大的影响胚胎死亡率和器官生长比缺氧发生在后期阶段（D 10至18）。心脏和绒毛尿囊膜的生长受到慢性缺氧的刺激，而肺、脑、眼、肝、胃、喙和脚趾没有受到破坏。从孵化开始持续缺氧降低血液血红蛋白，红细胞压积，和红细胞浓度的胚胎在第10天，但缺氧和常氧组之间的值在第18天没有显着差异。血液中的O-2分压和CO2分压依赖于孵育O-2水平在给定的一天的发展。这些结果表明，无论是在整个发育过程中的适度缺氧（15%O-2），或在任何水平的缺氧在后期阶段（d 11至18），增加心脏和绒毛尿囊膜的重量，这部分补偿缺氧对胚胎发育的不利影响。我们的结论是，胚胎发育的前半部分包含缺氧的不利影响的关键窗口，和后半部分包含的关键器官缺氧的补偿反应的关键窗口。
Hypoxia inhibits avian embryonic development, as well as increases embryonic mortality. However, the key organ systems affected by hypoxia, and their critical windows for development, are poorly understood. Consequently, chicken embryos were continuously exposed to 3 levels of oxygen (21, 15, or 13% O-2) throughout d 0 to 10, d 11 to 18, or d 0 to 18 of incubation, followed by morphometric and blood physiological measurements. Hypoxia occurring early during incubation (d 0 to 10) had larger effects on embryonic mortality and organ growth than hypoxia occurring at later stages (d 10 to 18). Growth of the heart and chorioallantoic membrane was stimulated by chronic hypoxia, whereas the lung, brain, eye, liver, stomach, beak, and toes showed no disruption. Sustained hypoxia from the beginning of incubation decreased blood hemoglobin, hematocrit, and red blood cell concentration of embryos at d 10, but the values among hypoxic and normoxic groups were not significantly different at d 18. Blood partial pressure of O-2 and partial pressure of CO2 were dependent upon incubation O-2 level at a given day of development. These results indicated that either modest hypoxia (15% O-2) throughout development, or hypoxia at any level during the late stages (d 11 to 18), increased the heart and chorioallantoic membrane weight, which partly compensated for the detrimental effects of hypoxia on embryonic development. We conclude that the first half of embryonic development contained the critical windows for the detrimental effects of hypoxia, and the second half contained the critical windows for the compensatory response of hypoxia in key organs.