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胚胎期缺氧会对成年普通鳄龟的餐后心血管功能进行编程()。

Embryonic hypoxia programmes postprandial cardiovascular function in adult common snapping turtles ().

作者信息

Wearing Oliver H, Conner Justin, Nelson Derek, Crossley Janna, Crossley Dane A

机构信息

Department of Biology, McMaster University, Hamilton, Ontario, Canada, L8S 4K1

Department of Biological Sciences, University of North Texas, Denton, TX 76203-5017, USA.

出版信息

J Exp Biol. 2017 Jul 15;220(Pt 14):2589-2597. doi: 10.1242/jeb.160549. Epub 2017 May 11.

DOI:10.1242/jeb.160549
PMID:28495871
Abstract

Reduced oxygen availability (hypoxia) is a potent stressor during embryonic development, altering the trajectory of trait maturation and organismal phenotype. We previously documented that chronic embryonic hypoxia has a lasting impact on the metabolic response to feeding in juvenile snapping turtles (). Turtles exposed to hypoxia as embryos [10% O (H10)] exhibited an earlier and increased peak postprandial oxygen consumption rate, compared with control turtles [21% O (N21)]. In the current study, we measured central blood flow patterns to determine whether the elevated postprandial metabolic response in H10 turtles is linked to lasting impacts on convective transport. Five years after hatching, turtles were instrumented to quantify systemic ([Formula: see text]) and pulmonary ([Formula: see text]) blood flows and heart rate () before and after a ∼5% body mass meal. In adult N21 and H10 turtles, was increased significantly by feeding. Although total stroke volume () remained at fasted values, this tachycardia contributed to an elevation in total cardiac output ([Formula: see text]). However, there was a postprandial reduction in a net left-right (L-R) shunt in N21 snapping turtles only. Relative to N21 turtles, H10 animals exhibited higher [Formula: see text] due to increased blood flow through the right systemic outflow vessels of the heart. This effect of hypoxic embryonic development, reducing a net L-R cardiac shunt, may support the increased postprandial metabolic rate we previously reported in H10 turtles, and is further demonstration of adult reptile cardiovascular physiology being programmed by embryonic hypoxia.

摘要

氧气供应减少(缺氧)是胚胎发育过程中的一种强大应激源,会改变性状成熟轨迹和生物体表型。我们之前记录到,慢性胚胎缺氧对幼年鳄龟进食后的代谢反应有持久影响()。与对照龟[21%氧气(N21)]相比,胚胎期暴露于缺氧环境[10%氧气(H10)]的龟在进食后表现出更早且更高的餐后耗氧率峰值。在本研究中,我们测量了中心血流模式,以确定H10龟餐后代谢反应升高是否与对对流运输的持久影响有关。孵化五年后,给龟安装仪器,以量化在摄入约5%体重的食物前后的全身([公式:见正文])和肺([公式:见正文])血流量以及心率()。在成年N21和H10龟中,进食显著增加了心率。尽管每搏输出量()保持在禁食时的值,但这种心动过速导致总心输出量([公式:见正文])升高。然而,仅在N21鳄龟中,进食后左右(L-R)净分流减少。相对于N21龟,H10动物由于通过心脏右体循环流出血管的血流量增加而表现出更高的[公式:见正文]。胚胎期缺氧发育减少心脏L-R净分流的这种效应,可能支持了我们之前报道的H10龟餐后代谢率升高的现象,并且进一步证明成年爬行动物的心血管生理是由胚胎期缺氧编程的。

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