Fetal cerebral oxygenation: the homeostatic role of vascular adaptations to hypoxic stress.

摘要: The mammalian fetus is highly adapted for growth in a low-O2 environment which arterial O2 tensions average near 30 mm Hg. Acute decreases tension below this value elicit vasodilatation, but the responses are blunted compared to those observed adults. Chronic hypoxia stimulates pattern of cerebrovascular remodeling that results an increased wall thickness and decreased overall contractility also depresses capacity cerebral vasodilatation through NO release, soluble guanylate cyclase activity, expression PKG substrates. Many these hypoxic effects appear be homeostatic may mediated by VEGFs, increase direct response and, turn, can dramatically alter function multiple contractile proteins smooth muscle both endothelium-dependent endothelium-independent on large artery muscle.