ReviewFrontiers in physiology2026
Enabling artificial placenta cannulation: mechanisms of postnatal umbilical vessel closure and strategies to prolong patency.
Review in Frontiers in physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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10 authors.
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Abstract
Umbilical vessel closure after birth prevents hemorrhage but limits the time window for large-bore umbilical cannulation required for artificial placenta support. This review synthesizes physiologic triggers, vasoactive pathways, and vessel-wall specializations that drive rapid postnatal occlusion and highlights engineering-relevant targets to prolong functional patency. Umbilical vessel closure is promoted by the transition to extrauterine life (cooling, rising oxygen tension, oxidative stress, loss of placental vasodilator influence), altered hemodynamics after lung aeration, and mechanical stimulation of the cord. At the molecular level, vasoconstriction is driven by redundant mediator networks-most prominently serotonin and thromboxane A
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