Nitric oxide dysregulation in the pathogenesis of preeclampsia among Ghanaian women

被引:13
作者
Adu-Bonsaffoh, Kwame [1 ,2 ]
Antwi, Daniel Ansong [1 ]
Obed, Samuel Amenyi [3 ]
Gyan, Ben [4 ]
机构
[1] Univ Ghana, Med Sch, Dept Physiol, Accra, Ghana
[2] Korle Bu Teaching Hosp, Dept Obstet & Gynecol, POB KB783, Accra, Ghana
[3] Univ Ghana, Sch Med, Dept Obstet & Gynecol, Accra, Ghana
[4] Univ Ghana, Noguchi Mem Inst Med Res, Dept Immunol, Accra, Ghana
来源
INTEGRATED BLOOD PRESSURE CONTROL | 2015年 / 8卷
关键词
preeclampsia; endothelial dysfunction; nitric oxide; Griess reagent;
D O I
10.2147/IBPC.S68454
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Background: Preeclampsia (PE) is still a disease of theories as the exact cause remains uncertain. Widespread vascular endothelial cell dysfunction is thought to mediate the generalized vasospasm and hypertension characteristic of PE. Altered nitric oxide (NO) production has been associated with the endothelial dysfunction in the pathogenesis of PE but conflicting results have emerged from previous studies. Objectives: To determine maternal serum levels of NO, a biomarker of endothelial function, in nonpregnant, normal pregnant, and preeclamptic women. Materials and methods: This was a cross-sectional case-control study of 277 women comprising 75 nonpregnant, 102 normal pregnant, and 100 preeclamptic women conducted at the Korle Bu Teaching Hospital between April and June 2011. About 5 mL of venous blood was obtained from the participants for the various investigations after meeting the inclusion criteria and signing to a written consent. Serum levels of NO were determined by Griess reaction. The data obtained were analyzed with SPSS version 20. Results: The study showed significantly elevated serum levels of NO in preeclamptic women (82.45 +/- 50.31 mu M) compared with normal pregnant (33.12 +/- 17.81 mu M) and nonpregnant (16.92 +/- 11.41 mu M) women with P<0.001. The alteration in maternal serum NO levels was significantly more profound in early-onset (severe) PE (119.63 +/- 45.860 mu M) compared to that of late-onset (mild) disease (62.44 +/- 40.44 mu M) with P<0.001, indicating a more severe vascular endothelial cell dysfunction in the early-onset disease. Conclusion: This study has determined a profound NO upregulation in PE evidenced by significant elevation of NO metabolite levels compared to normal pregnancy. This might be due to deranged endothelial function with dysregulated production of NO to restore the persistent hypertension characteristic of PE.
引用
收藏
页码:1 / 6
页数:6
相关论文
共 22 条
  • [1] ACOG, 2002, ACOG PRACT B, P33
  • [2] Maternal deaths attributable to hypertensive disorders in a tertiary hospital in Ghana
    Adu-Bonsaffoh, Kwame
    Samuel, Oppong A.
    Binlinla, Godwin
    Samuel, Obed A.
    [J]. INTERNATIONAL JOURNAL OF GYNECOLOGY & OBSTETRICS, 2013, 123 (02) : 110 - 113
  • [3] The nitric oxide pathway in pre-eclampsia: pathophysiological implications
    Buhimschi, IA
    Saade, GR
    Chwalisz, K
    Garfield, RE
    [J]. HUMAN REPRODUCTION UPDATE, 1998, 4 (01) : 25 - 42
  • [4] Choi JW, 2002, ANN CLIN LAB SCI, V32, P2002
  • [5] NOS EXPRESSION IS INCREASED IN ENDOTHELIAL-CELLS EXPOSED TO PLASMA FROM WOMEN WITH PREECLAMPSIA
    DAVIDGE, ST
    BAKER, PN
    ROBERTS, JM
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1995, 269 (03): : H1106 - H1112
  • [6] Urine but not plasma nitric oxide metabolites are decreased in women with preeclampsia
    Davidge, ST
    Stranko, CP
    Roberts, JM
    [J]. AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1996, 174 (03) : 1008 - 1013
  • [7] Diejomaoh F. M. E., 2004, Archives of Gynecology and Obstetrics, V269, P237
  • [8] Preeclampsia 2012
    Eiland, Elosha
    Nzerue, Chike
    Faulkner, Andmarquetta
    [J]. JOURNAL OF PREGNANCY, 2012, 2012
  • [9] George EM, 2012, EXPERT REV OBSTET GY, V5, P557
  • [10] Pathophysiology of hypertension during preeclampsia: linking placental ischemia with endothelial dysfunction
    Gilbert, Jeffrey S.
    Ryan, Michael J.
    LaMarca, Babbette B.
    Sedeek, Mona
    Murphy, Sydney R.
    Granger, Joey P.
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2008, 294 (02): : H541 - H550