Koos Brian J, Maeda Takatsugu, Jan Calvin, Lopez Grace
Nicholas S. Assali Perinatal Research Laboratory, Department of Obstetrics and Gynecology, Brain Research Institute, University of California, Los Angeles School of Medicine, 90095-1740, USA..
Am J Obstet Gynecol. 2002 Apr;186(4):663-8. doi: 10.1067/mob.2002.122129.
Hypoxia inhibits fetal breathing through activation of central adenosine (ADO) receptors that modulate fetal behavioral state. This study was designed to determine whether adenosine A(1) and/or A(2A)receptor subtypes mediate the depressant effects of hypoxia.
In 14 chronically catheterized fetal sheep (>0.8 term), hypoxemia was induced by having the ewe breathe a gas mixture of 9% oxygen for 1 hour. During hypoxia, the fetus was infused intra-arterially with a vehicle or an antagonist for adenosine A(1) or A(2A) receptors. Statistical analysis was performed by using analysis of variance with Tukey's least significant difference criterion.
Fetal isocapnic hypoxemia (PaO(2): control, approximately 24 mm Hg; hypoxia, approximately 14 mm Hg) virtually eliminated rapid eye movements and breathing when the fetus was infused with vehicle or the A(1) receptor antagonist. In contrast, adenosine A(2A) receptor blockade abolished the hypoxia-induced arrest of rapid eye movements and breathing.
Hypoxic inhibition of rapid eye movements and breathing is critically dependent on activation of adenosine A(2A) receptors.
缺氧通过激活调节胎儿行为状态的中枢腺苷（ADO）受体来抑制胎儿呼吸。本研究旨在确定腺苷A(1)和/或A(2A)受体亚型是否介导缺氧的抑制作用。
在14只长期插管的胎羊（胎龄>0.8）中，通过让母羊呼吸含9%氧气的混合气体1小时来诱导低氧血症。在缺氧期间，经动脉向胎儿输注载体或腺苷A(1)或A(2A)受体拮抗剂。采用方差分析和Tukey最小显著差异标准进行统计分析。
当给胎儿输注载体或A(1)受体拮抗剂时，胎儿等碳酸血症性低氧血症（动脉血氧分压：对照组约24 mmHg；缺氧组约14 mmHg）几乎消除了快速眼动和呼吸。相比之下，腺苷A(2A)受体阻断消除了缺氧诱导的快速眼动和呼吸停止。
缺氧对快速眼动和呼吸的抑制作用严重依赖于腺苷A(2A)受体的激活。
