• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

慢性缺氧对胎儿冠状动脉反应的影响。

Effects of chronic hypoxia on fetal coronary responses.

作者信息

Thompson Loren P

机构信息

Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, MD, USA.

出版信息

High Alt Med Biol. 2003 Summer;4(2):215-24. doi: 10.1089/152702903322022811.

DOI:10.1089/152702903322022811
PMID:12855053
Abstract

This review examines the effect of high altitude and/or chronic hypoxia on cardiac mechanisms that influence perfusion of the fetal heart (e.g., tissue metabolism, coronary vessel growth, and coronary blood flow and vessel responsiveness). In response to intrauterine hypoxia, the fetal heart may either reduce its energy demand or increase its substrate and oxygen delivery as a means of sustaining cardiac function. Cardiac glycolysis predominates as a metabolic pathway of ATP synthesis in the fetal heart under both normoxic and hypoxic conditions. During prolonged oxygen insufficiency, normal cardiac function is sustained by anaerobic glycolysis relying primarily on high levels of stored glycogen in the heart. Chronic hypoxia increases coronary vessel growth and myocardial vascularization in fetal hearts, although the response may depend on the presence of ventricular hypertrophy. Recent studies demonstrate that high altitude hypoxia increases both resting fetal coronary flow and coronary flow reserve as an adaptive response toward increasing oxygen delivery. Hypoxia may also directly effect local vascular smooth muscle mechanisms, resulting in altered coronary artery reactivity to circulating vasoactive substances and contributing to enhanced perfusion. Further study is needed to understand the relative importance of each of these cardiac adaptations in contributing to fetal survival. It is likely that differences in fetal coronary responses to intrauterine hypoxia are highly dependent on the gestational age and relative maturity of the animal species.

摘要

本综述探讨了高海拔和/或慢性缺氧对影响胎儿心脏灌注的心脏机制的作用(例如,组织代谢、冠状动脉生长、冠状动脉血流及血管反应性)。为应对宫内缺氧,胎儿心脏可能会降低其能量需求,或增加其底物和氧气供应,以此维持心脏功能。在常氧和缺氧条件下,心脏糖酵解均是胎儿心脏中ATP合成的主要代谢途径。在长时间缺氧期间,心脏主要依靠高水平储存的糖原通过无氧糖酵解来维持正常心脏功能。慢性缺氧会增加胎儿心脏的冠状动脉生长和心肌血管生成,不过这种反应可能取决于心室肥大的存在。最近的研究表明,高海拔缺氧会增加胎儿静息冠状动脉血流和冠状动脉血流储备,作为对增加氧气供应的适应性反应。缺氧还可能直接影响局部血管平滑肌机制,导致冠状动脉对循环血管活性物质的反应性改变,并有助于增强灌注。需要进一步研究以了解这些心脏适应性变化各自对胎儿存活的相对重要性。胎儿冠状动脉对宫内缺氧的反应差异很可能高度依赖于动物物种的胎龄和相对成熟度。

相似文献

1
Effects of chronic hypoxia on fetal coronary responses.慢性缺氧对胎儿冠状动脉反应的影响。
High Alt Med Biol. 2003 Summer;4(2):215-24. doi: 10.1089/152702903322022811.
2
Regulation of coronary blood flow during exercise.运动期间冠状动脉血流的调节。
Physiol Rev. 2008 Jul;88(3):1009-86. doi: 10.1152/physrev.00045.2006.
3
Hypoxic induction of myocardial vascularization during development.
Adv Exp Med Biol. 2003;543:139-49. doi: 10.1007/978-1-4419-8997-0_10.
4
Differential expression of endothelial nitric oxide synthase in coronary and cardiac tissue in hypoxic fetal guinea pig hearts.缺氧胎豚鼠心脏中冠状动脉和心肌组织内皮型一氧化氮合酶的差异表达
J Soc Gynecol Investig. 2006 Oct;13(7):483-90. doi: 10.1016/j.jsgi.2006.06.005. Epub 2006 Sep 18.
5
Cardiac myocyte-specific HIF-1alpha deletion alters vascularization, energy availability, calcium flux, and contractility in the normoxic heart.心肌细胞特异性缺氧诱导因子-1α缺失会改变正常氧合心脏中的血管生成、能量供应、钙通量和收缩性。
FASEB J. 2004 Jul;18(10):1138-40. doi: 10.1096/fj.04-1510fje. Epub 2004 May 7.
6
The effect of long-term hypoxia on tension and intracellular calcium responses following stimulation of the thromboxane A(2) receptor in the left anterior descending coronary artery of fetal sheep.长期缺氧对胎羊左前降支冠状动脉血栓素A(2)受体刺激后张力及细胞内钙反应的影响。
Reprod Sci. 2009 Apr;16(4):364-72. doi: 10.1177/1933719109333439.
7
Metabolic changes in the normal and hypoxic neonatal myocardium.正常和缺氧新生儿心肌的代谢变化。
Ann N Y Acad Sci. 1999 Jun 30;874:254-61. doi: 10.1111/j.1749-6632.1999.tb09240.x.
8
Hypoxia and fetal heart development.缺氧与胎儿心脏发育。
Curr Mol Med. 2010 Oct;10(7):653-66. doi: 10.2174/156652410792630643.
9
Abnormal myocardial and coronary vasculature development in experimental hypoxia.实验性低氧状态下心肌和冠状血管的异常发育
Anat Rec (Hoboken). 2008 Oct;291(10):1187-99. doi: 10.1002/ar.20738.
10
Tribute to P. L. Lutz: a message from the heart--why hypoxic bradycardia in fishes?向P.L. 卢茨致敬:发自内心的讯息——鱼类为何会出现低氧性心动过缓?
J Exp Biol. 2007 May;210(Pt 10):1715-25. doi: 10.1242/jeb.02781.

引用本文的文献

1
Molecular and Biochemical Mechanisms of Cardiomyopathy Development Following Prenatal Hypoxia-Focus on the NO System.产前缺氧后心肌病发展的分子和生化机制——聚焦于一氧化氮系统
Antioxidants (Basel). 2025 Jun 16;14(6):743. doi: 10.3390/antiox14060743.
2
WNT5A, β‑catenin and SUFU expression patterns, and the significance of microRNA deregulation in placentas with intrauterine growth restriction.WNT5A、β-连环蛋白和 SUFU 的表达模式,以及宫内生长受限胎盘中小分子 RNA 失调的意义。
Mol Med Rep. 2023 Feb;27(2). doi: 10.3892/mmr.2022.12914. Epub 2022 Dec 16.
3
Gestational Hypoxia and Programing of Lung Metabolism.
妊娠期缺氧与肺代谢编程
Front Physiol. 2019 Nov 29;10:1453. doi: 10.3389/fphys.2019.01453. eCollection 2019.
4
Fetal in vivo continuous cardiovascular function during chronic hypoxia.慢性缺氧期间胎儿体内连续的心血管功能
J Physiol. 2016 Mar 1;594(5):1247-64. doi: 10.1113/JP271091.
5
The energetics of CNS white matter.中枢神经系统白质的能量学。
J Neurosci. 2012 Jan 4;32(1):356-71. doi: 10.1523/JNEUROSCI.3430-11.2012.
6
Causes and mechanisms of intrauterine hypoxia and its impact on the fetal cardiovascular system: a review.宫内缺氧的原因、机制及其对胎儿心血管系统的影响:综述
Int J Pediatr. 2010;2010:401323. doi: 10.1155/2010/401323. Epub 2010 Oct 19.
7
Chronic hypoxia increases inducible NOS-derived nitric oxide in fetal guinea pig hearts.慢性低氧血症会增加胎豚鼠心脏中诱导型一氧化氮合酶衍生的一氧化氮。
Pediatr Res. 2009 Feb;65(2):188-92. doi: 10.1203/PDR.0b013e31818d6ad0.