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Increased microvascular vasodilation and cardiovascular risk following a pre-eclamptic pregnancy.

Murphy MS, Vignarajah M, Smith GN - Physiol Rep (2014)

Bottom Line: Acetylcholine-mediated vasodilation was enhanced by normotensive pregnancy, and declined to nonpregnant levels by 6 months postpartum.Acetylcholine-mediated vasodilation remained high in pre-eclamptic subjects from 2 to 6 months postpartum compared to normotensive and never-pregnant controls.Pre-eclamptic subjects exhibited elevated 30-year and lifetime risk at 6 months postpartum.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical and Molecular Science, Queen's University, Kingston, Ontario, Canada.

No MeSH data available.


Related in: MedlinePlus

Endothelial‐dependent responses to ACh and endothelial‐independent responses to SNP in normotensive women (n = 23) in the third trimester (3TM), 6 weeks postpartum (6W PP) and 6 months postpartum (6M PP) compared to never‐pregnant (NP, n = 15) subjects. Data are presented as mean ± SEM. Post hoc comparisons*P < 0.001 3TM versus 6M PP; †P < 0.05 3TM versus NP; ‡P < 0.05, 6W PP versus 6M PP.
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fig02: Endothelial‐dependent responses to ACh and endothelial‐independent responses to SNP in normotensive women (n = 23) in the third trimester (3TM), 6 weeks postpartum (6W PP) and 6 months postpartum (6M PP) compared to never‐pregnant (NP, n = 15) subjects. Data are presented as mean ± SEM. Post hoc comparisons*P < 0.001 3TM versus 6M PP; †P < 0.05 3TM versus NP; ‡P < 0.05, 6W PP versus 6M PP.

Mentions: Microvascular measurements taken in 23 (n = 23) normotensive pregnant controls demonstrated that the third trimester of pregnancy was associated with enhanced endothelial‐dependent vasodilation in response to ACh (P < 0.0001) compared to never‐pregnant levels. This effect persisted at 6 weeks postpartum. Microvascular reactivity returned to levels similar to never‐pregnant controls by 6 months postpartum (P > 0.05). Microvascular responses to SNP were unchanged in pregnancy and in the postpartum (P > 0.05) (Fig. 2).


Increased microvascular vasodilation and cardiovascular risk following a pre-eclamptic pregnancy.

Murphy MS, Vignarajah M, Smith GN - Physiol Rep (2014)

Endothelial‐dependent responses to ACh and endothelial‐independent responses to SNP in normotensive women (n = 23) in the third trimester (3TM), 6 weeks postpartum (6W PP) and 6 months postpartum (6M PP) compared to never‐pregnant (NP, n = 15) subjects. Data are presented as mean ± SEM. Post hoc comparisons*P < 0.001 3TM versus 6M PP; †P < 0.05 3TM versus NP; ‡P < 0.05, 6W PP versus 6M PP.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255821&req=5

fig02: Endothelial‐dependent responses to ACh and endothelial‐independent responses to SNP in normotensive women (n = 23) in the third trimester (3TM), 6 weeks postpartum (6W PP) and 6 months postpartum (6M PP) compared to never‐pregnant (NP, n = 15) subjects. Data are presented as mean ± SEM. Post hoc comparisons*P < 0.001 3TM versus 6M PP; †P < 0.05 3TM versus NP; ‡P < 0.05, 6W PP versus 6M PP.
Mentions: Microvascular measurements taken in 23 (n = 23) normotensive pregnant controls demonstrated that the third trimester of pregnancy was associated with enhanced endothelial‐dependent vasodilation in response to ACh (P < 0.0001) compared to never‐pregnant levels. This effect persisted at 6 weeks postpartum. Microvascular reactivity returned to levels similar to never‐pregnant controls by 6 months postpartum (P > 0.05). Microvascular responses to SNP were unchanged in pregnancy and in the postpartum (P > 0.05) (Fig. 2).

Bottom Line: Acetylcholine-mediated vasodilation was enhanced by normotensive pregnancy, and declined to nonpregnant levels by 6 months postpartum.Acetylcholine-mediated vasodilation remained high in pre-eclamptic subjects from 2 to 6 months postpartum compared to normotensive and never-pregnant controls.Pre-eclamptic subjects exhibited elevated 30-year and lifetime risk at 6 months postpartum.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedical and Molecular Science, Queen's University, Kingston, Ontario, Canada.

No MeSH data available.


Related in: MedlinePlus