title: Erythrocyte sodium lithium countertransport in normal and hypertensive pregnancy: relation to haemodynamic changes.
abstract: OBJECTIVE
  To establish the changes in erythrocyte sodium lithium countertransport (SLC) with advancing normal pregnancy and to determine if these changes were different in pregnancy induced hypertension (PIH). The changes in both groups were assessed in relation to haemodynamic changes.
  
  
  METHODS
  SLC, mean arterial pressure (MAP), cardiac output (CO) and total peripheral vascular resistance (TPVR) were determined serially during normal pregnancy and cross-sectionally in PIH. Women were studied again 20 weeks after delivery where possible.
  
  
  METHODS
  Routine antenatal clinic and antenatal ward of a regional reference centre.
  
  
  METHODS
  Fifty-one normal primigravid women were studied serially and 41 primigravid women with PIH were studied at time of diagnosis.
  
  
  RESULTS
  During normal pregnancy SLC (mmol Li/h/l cells) increased from a nonpregnant value of 0.24 +/- 0.02 (mean +/- SEM) to 0.32 +/- 0.02 at 14 weeks, and 0.37 +/- 0.02 at 20 weeks gestation. This was maintained until 38 weeks (0.40 +/- 0.02). The increase until 20 weeks occurred at the time of greatest change in CO (5.10 +/- 0.18 to 6.79 +/- 0.20 l/min) and TPVR (1327 +/- 58 to 969 +/- 33 dyn/s/cm-5). The decrease in TPVR with a rise in SLC is opposite to the relation reported in essential hypertension so that a functional relation is unlikely. However, the changes within pregnancy were positively correlated (r = 0.43, P < 0.01). In hypertensive pregnancies TPVR was elevated compared with normotensive pregnancies (1543 +/- 100 vs 1090 +/- 37) but the SLC was not different from that found in normotensive pregnancies (0.43 +/- 0.02 vs 0.40 +/- 0.02).
  
  
  CONCLUSIONS
  The changes in SLC activity suggest dynamic effects on erythrocyte membrane function during pregnancy. However, no differences could be found between normal and hypertensive pregnancy and SLC is unlikely to be of value as a marker of hypertensive risk during pregnancy.
authors.affiliation: Department of Obstetrics and Gynaecology, University of Newcastle upon Tyne, UK.
authors.forename: S
authors.initials: S
authors.lastname: Macphail
authors.forename: T H
authors.initials: TH
authors.lastname: Thomas
authors.forename: R
authors.initials: R
authors.lastname: Wilkinson
authors.forename: J M
authors.initials: JM
authors.lastname: Davison
authors.forename: W
authors.initials: W
authors.lastname: Dunlop
mesh_terms: D000328:Adult; D017920:Antiporters; D001794:Blood Pressure; D002302:Cardiac Output; D002352:Carrier Proteins / Q000378:metabolism*; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D011247:Pregnancy / Q000378:metabolism*; D011249:Pregnancy Complications, Cardiovascular / Q000378:metabolism* / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D017920:Antiporters; D002352:Carrier Proteins; C045885:sodium-lithium countertransporter