2004
DOI: 10.1016/j.athoracsur.2004.05.057
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Impaired Endothelial Function of the Umbilical Artery After Fetal Cardiac Bypass

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Cited by 9 publications
(9 citation statements)
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“…These might be related to the pathophysiological changes of fetal cardiac bypass. Previous studies demonstrated that fetal cardiac bypass increased placental vascular resistance through a variety of vasoconstrictor and cytokines (8,9). We also showed evidence of increase in placental vascular resistance after cardiac bypass, which increased the afterload of fetal right ventricle and reduced placental gas exchange function.…”
Section: Discussionsupporting
confidence: 72%
See 1 more Smart Citation
“…These might be related to the pathophysiological changes of fetal cardiac bypass. Previous studies demonstrated that fetal cardiac bypass increased placental vascular resistance through a variety of vasoconstrictor and cytokines (8,9). We also showed evidence of increase in placental vascular resistance after cardiac bypass, which increased the afterload of fetal right ventricle and reduced placental gas exchange function.…”
Section: Discussionsupporting
confidence: 72%
“…Establishment of a safe fetal cardiac bypass is thus a prerequisite for fetal cardiac surgery. However, early studies demonstrated that fetal cardiac bypass could be detrimental to placental function (5–9), and placental insufficiency could compromise fetal cardiac function (10). We hypothesized that fetal cardiac bypass influenced the secretion of ANP and fetal cardiac function following the bypass.…”
mentioning
confidence: 98%
“…In previous CPB ovine fetal models, the placenta served as the sole oxygenator, resulting in unstable oxygenation and severe placental damage occurring (24,25). It was observed that inhibiting stress and protecting vascular endothelial function of the placenta following CPB prevented an increase in the vascular resistance of the placenta that would otherwise lead to impairment of placental function, irreversible acidosis and subsequent fetal death (24).…”
Section: Discussionmentioning
confidence: 99%
“…In previous CPB ovine fetal models, the placenta served as the sole oxygenator, resulting in unstable oxygenation and severe placental damage occurring (24,25). It was observed that inhibiting stress and protecting vascular endothelial function of the placenta following CPB prevented an increase in the vascular resistance of the placenta that would otherwise lead to impairment of placental function, irreversible acidosis and subsequent fetal death (24). During CPB, the following typically influence the extent of placental damage: i) Re-distribution of fetal blood flow, ii) placental vascular endothelial dysfunction, iii) humoral factors, iv) perfusion patterns, v) pre-perfusion solution, and vi) low temperatures (25).…”
Section: Discussionmentioning
confidence: 99%
“…They release NO to regulate the tension of umbilical vessels, and mitigate the constrictive effect of embroxane and endothelin. [9] Oishi et al [10] found that increased umbilical artery resistance is due to deterioration of the endothelium dependent vasodilator effect. The endothelium independent vasodilator (nitroprusside) function is not altered.…”
Section: Shanghai Chinamentioning
confidence: 99%