Center for Cardiovascular Research, Prague, Czech Republic.
Physiol Res. 2009;58 Suppl 2:S87-S94. doi: 10.33549/physiolres.931922.
Important fetal and perinatal pathologies, especially intrauterine growth restriction (IUGR), are thought to stem from placental hypoxia-induced vasoconstriction of the fetoplacental vessels, leading to placental hypoperfusion and thus fetal undernutrition. However, the effects of hypoxia on the fetoplacental vessels have been surprisingly little studied. We review here available experimental data on acute hypoxic fetoplacental vasoconstriction (HFPV) and on chronic hypoxic elevation of fetoplacental vascular resistance. The mechanism of HFPV includes hypoxic inhibition of potassium channels in the plasma membrane of fetoplacental vascular smooth muscle and consequent membrane depolarization that activates voltage gated calcium channels. This in turn causes calcium influx and contractile apparatus activation. The mechanism of chronic hypoxic elevation of fetoplacental vascular resistance is virtually unknown except of signs of the involvement of morphological remodeling.
重要的胎儿和围产期病理学，特别是宫内生长受限（IUGR），被认为源于胎盘缺氧诱导的胎儿胎盘血管收缩，导致胎盘灌注不足，从而导致胎儿营养不良。然而，缺氧对胎儿胎盘血管的影响却出人意料地研究甚少。我们在此回顾了关于急性缺氧胎儿胎盘血管收缩（HFPV）和慢性缺氧胎儿胎盘血管阻力升高的现有实验数据。HFPV 的机制包括缺氧抑制胎儿胎盘血管平滑肌细胞膜上的钾通道，继而引起膜去极化，激活电压门控钙通道。这反过来又导致钙内流和收缩装置的激活。除了形态重塑参与的迹象外，慢性缺氧导致胎儿胎盘血管阻力升高的机制实际上还不清楚。
