Skip to main content

Advertisement

SpringerLink
Log in

Relationship of Cell Adhesion Molecule Expression to Endothelium-Dependent Relaxation in Normal Pregnancy and Pregnancies Complicated With Preeclampsia or Fetal Growth Restriction

  • Original Articles
  • Published:
The Journal of the Society for Gynecologic Investigation: JSGI Aims and scope Submit manuscript

Abstract

Objectives

To determine the degree of endothelium-dependent relaxation in myometrial and omental resistance arteries from normal pregnancies and pregnancies complicated with preeclampsia or fetal growth restriction (FGR) (compromised pregnancy group), and to correlate the results with the endothelial surface expression of cell adhesion molecules (CAMs) in the same vessels.

Methods

Parallel wire myograph was used to assess the relaxation of omentum or myomentrial vessels obtained from monpregnant women (n = 3), women with normal pregnancies (n = 11), and women with pregnancies complicated by preeclampsia or fetal growth restriction (n = 10). These resistance vessels were constricted with incremental concentrations of vasopressin (10-10 mol/L to 3.3 × 10-8 mol/L) prior to the addition of incremental concentrations of bradykinin (10-10 mol/L to 3.3 × 10-6 mol/L). Immunohistochemistry was used to assess the endothelial expression of the CAMs E-selectin, ICAM-1, VCAM-1, and PECAM.

Results

A significant reduction in endothelium-dependent relaxation of myometrial vessels was found in the compromised pregnancy group when compared with both the normotensive pregnant group and the nonpregnant group. This reduction was not noted with omenal vessels. All vessels in the nonpregnant group, normal pregnant group, and compromised pregnancy group expressed PECAM and ICAM-1 on the endothelium. There was no difference in intensity of immunostaining between the groups. None of the vessels in any of the groups expressed VCAM-1 or E-selectin.

Conclusions

We found no evidence that impaired relaxation responses to bradykinin are linked to altered expression of CAMs in preeclampsia and FGR. These results suggest that increased CAM expression occurs in a vascular bed separate from those investigated in the present study. Possible sites for his would be in the microcirculation of organs such as the kidney.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  1. Lewis G, Drife JO. Why mothers die. Report on confidential enquiries into maternal deaths in the United Kingdom, 1094–1996. London: Department of Health. Welsh Office. Scottish Office Department of Health. Department of Health and Social Services, Northern Ireland, 1998.

    Google Scholar 

  2. Hibbard M, Anderson MM, Drife JO. Report on confidential enquiries into maternal deaths in the United Kingdom, 1991−1993. London: HMSO, 1995.

    Google Scholar 

  3. Scott A, Moar V, Ounstead M. The relative contribution of different maternal factors in small-for-gestational age pregnancies. Eur J Obstet Gynecol Reprod Biol 1981;12:157−65.

    Article  CAS  Google Scholar 

  4. Lunell NO, Sarby B, Lewander R, Nylund L. Comparison of uteroplacental blood flow in normal and intrauterine growth-retarded pregnancy. Gynecol Obstet Invest 1979;10:106−18.

    Article  CAS  Google Scholar 

  5. Lunell NO, Nylund LE, Lewander R, Sarby B. Uteroplacental blood flow in pre-eclampsia. Measurements with indium-113m and a computer-linked gamma camera. Clin Exp Hypertens 1982;B1:105−17.

    Google Scholar 

  6. Khong TY, De Wolf F, Robertson WB, Brosens I. Inadequate maternal vascular response to placentation in pregnancies complicated by pre-eclampsia and by small-for-gestational age infants. Br J Obstet Gynaecol 1986;93:1049−59.

    Article  CAS  Google Scholar 

  7. Pijnenborg R, Anthony J, Davey DA, et al. Placental bed spiral arteries in the hypertensive disorders of pregnancy. Br J Obstet Gynaecol 1991;98:648−55.

    Article  CAS  Google Scholar 

  8. Roberts JM, Redman CW. Pre-eclampsia: More than pregnancy-induced hypertension. Lancet 1993;341:1447−51.

    Article  CAS  Google Scholar 

  9. Lyall F, Greer IA. The vascular endothelium in normal pregnancy and pre-eclampsia. Rev Reprod 1996;1:107–16.

    Article  CAS  Google Scholar 

  10. Lyall F. Cell adhesion molecules: Their role in pregnancy. Fetal and Maternal Medicine Review 1998;10:21–44.

    Article  Google Scholar 

  11. Gearing AJH, Memingway I, Piggot R, Hughes J, Rees AJ, Cashman SJ. Soluble forms of adhesion molecules, E-Selectin, ICAM-1 and VCAM-1: Pathological significance. Ann New-York Acad Sci 1992;667:324–31.

    Article  CAS  Google Scholar 

  12. Lyall F, Greer IA. The cell adhesion molecule VCAM-1 is selectively increased in serum in pre-eclampsia: Does this indicate the mechanism of neutrophil activation? [letter]. Br J Obstet Gynaecol 1995;102:173–4.

    Article  Google Scholar 

  13. Lyall F, Greer IA, Boswell F, Macara LM, Walker JJ, Kingdom JCP. The cell adhesion molecule VCAM-1 is selectively increased in serum in pre-eclampsia: Does this indicate the mechanism of neutrophil activation? Br J Obstet Gynaecol 1994;101:485–7.

    Article  CAS  Google Scholar 

  14. Ashworth JR, Warrern AY, Baker PN, Johnson IR. Loss of endothelium-dependent relaxation in myometrial resistance arteries in pre-eclampsia. Br J Obstet Gynaecol 1997;104:1152–8.

    Article  CAS  Google Scholar 

  15. Ashworth JR, Warren AY, Baker PN, Johnson IR. Altered endothelium-dependent relaxation in myometrial resistance arteries in pre-eclampsia and intrauterine growth retardation. J Vasc Res 1996;33 Suppl 2:35.

    Google Scholar 

  16. Baker PN, Ashworth JR. Warren AY, Johnson IR. Pre-eclampsia and intrauterine growth retardation: A common pathogenesis involving the human myometrial resistance arteries. Hypertens Preg 1997;16:90.

    Article  Google Scholar 

  17. Rodgers GM, Taylor RM, Roberts JM. Preeclampsia is associated with a serum factor cyto-toxic to human endothelial cells. Am J Obstet Gynecol 1988;158:908–14.

    Article  Google Scholar 

  18. Davey DA, MacGillivray I. The classification of the hypertensive diorders of pregnancy. Am J Obstet Gynecol 1988;158:892–8.

    Article  CAS  Google Scholar 

  19. Gardosi J, Chang A, Kalyan B, Sahota D, Symonds EM. Customized antenatal growth charts. Lancet 1992;339:283–7.

    Article  CAS  Google Scholar 

  20. Wilcox AJ, Weinberg CR, O’Connor JF, et al. Incidence of early pregnancy loss. N Engl J Med 1988;319:189–94.

    Article  CAS  Google Scholar 

  21. Aalkjaer C, Danielsen H. Johannesen P, Pedersen EB, Rasmussen A, Mulvanv MJ. Abnormal vascular function and morphology in pre-eclampsia: A study of isolated resistance vessels. Clin Sci 1985;69:477–82.

    Article  Google Scholar 

  22. Mulvany MJ, Halpen W. Mechanical properties of vascular smooth muscle cells in situ. Nature 1976;260:617–9.

    Article  CAS  Google Scholar 

  23. Lyall F, Boswell F, Young A, Clark CJ, Greer IA. The cytokine interleukin-6 increases expression of the cell adhesion molecule E-selectin and VCAM-1 on endothelial cells in vitro: A role in pre-eclampsia? Hypertens Preg 1997;16:403–15.

    Article  CAS  Google Scholar 

  24. Wang Y. Adair D, Coe L. Weeks JW, Lewis DF, Alexander JS. Activation of endothelial cells in preeclampsia: Increased neutrophil-endothclial adhesion correlates with up-regulation of adhesion molecules P-Selectin in human umbilical vein endothelial cells isolated from preeclampsia. J Soc Gynecol Invest 1998;5:237–43.

    CAS  Google Scholar 

  25. Djurovic S, Schjetlein R, Wisloff F, Haugen G, Berg K. Increased levels of intercellular adhesion molecules and vascular cell adhesion molecules in pre-eclampsia. Br J Obstet Gynaecol 1997;104:466–70.

    Article  CAS  Google Scholar 

  26. Krauss T, Kuhn W, Lakoma C, Augustin HG. Circulating endothelial cell adhesion molecules as diagnostic markers for the early identification of pregnant women at risk for development of preeclampsia. Am J Obstet Gynecol 1997;177:443–9.

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Maternal and Fetal Medicine Section, University of Glasgow Institute of Medical Genetics, Yorkhill, Glasgow, 3D 8SJ, United Kingdom

    Fiona Lylla PhD, Richard G. Hayman MRCOG, Janet R. Ashworth MD, Elizabeth Duffie & Philip N. Baker MD

  2. School of Human Development, University of Nottingham, Nottingham, United Kingdom

    Fiona Lylla PhD, Richard G. Hayman MRCOG, Janet R. Ashworth MD, Elizabeth Duffie & Philip N. Baker MD

Authors
  1. Fiona Lylla PhD
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Richard G. Hayman MRCOG
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Janet R. Ashworth MD
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Elizabeth Duffie
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Philip N. Baker MD
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Fiona Lylla PhD.

Additional information

Supported by the British Heart Foundation and Tommy’s Campaign.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Lylla, F., Hayman, R.G., Ashworth, J.R. et al. Relationship of Cell Adhesion Molecule Expression to Endothelium-Dependent Relaxation in Normal Pregnancy and Pregnancies Complicated With Preeclampsia or Fetal Growth Restriction. Reprod. Sci. 6, 196–201 (1999). https://doi.org/10.1177/107155769900600406

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1177/107155769900600406

Key words

Search

Navigation