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Notes: Objectives To determine whether the change in erythrocyte potassium content in normal human pregnancy is accompanied by a similar change in erythrocyte chloride content. To assess erythrocyte hydration and potassium and chloride content in pregnancies complicated by proteinuric pregnancy induced hypertension.Design A serial study during and after normal pregnancy. A comparative study during and after pregnancies complicated by proteinuric pregnancy induced hypertension (PIH). Erythrocyte hydration, total osmoles, potassium and chloride and plasma osmolality were determined.Setting University teaching hospital, UK.Subjects Twenty-eight women studied at 14, 28 and 36 weeks of normal pregnancy and ten women with PIH studied during the third trimester of pregnancy. All women were reinvestigated 20 weeks after delivery.Results The fall of erythrocyte potassium early in normal pregnancy (277.4 vs 265.2 mmol/kg; P〈0.02) and its rise between 28 and 36 weeks (272.3 vs 288.0 mmol/kg; P〈0.005) were accompanied by similar changes in erythrocyte chloride content (151.9 vs 131.1 mmol/kg; P〈0.001 and 129.4 vs 141.3 mmol/kg; P〈0.001, respectively). Plasma osmolality in PIH was raised above that normal in pregnancy (287.2 vs 283.0 mosm/kg; P〈0.005). In PIH, compared to normal pregnancy, erythrocyte hydration (2.00 vs 1.89 l/kg dry weight cells), total osmoles (573.0 vs 534.2 mosm/kg), potassium (303.0 vs 288.0 mmol/kg) and chloride (154.9 vs 141.3 mmol/kg) were greater.Conclusions These findings further support the hypothesis that changes in plasma osmolality in pregnancy are secondary to alterations in cell osmoles and serve to limit changes in cell hydration. Erythrocyte composition and plasma osmolality are altered in PIH.

Notes: Objective To determine the effect of early labour, maternal analgesia and fetal hypoxia on circulating fetal oxytocin concentrations.Design Prospective observational study.Setting Delivery suite in a District General Hospital.Subjects Fifty women at term who did not require oxytocin administration or more than one form of analgesia. Study groups: vaginal delivery with (1) no analgesia, (2) pethidine, or (3) epidural analgesia. Caesarean section under regional analgesia (4) prior to, and (5) after the onset of labour.Interventions Samples of blood were collected from the umbilical artery (UA) and umbilical vein (UV) immediately after fetal delivery prior to placental separation or oxytocic administration.Main outcome measures Plasma oxytocin (OT) concentration, umbilical vein pH, cystine aminopeptidase activity.Results The geometric mean UA–OT was significantly greater than UV–OT in all groups and was not altered by pethidine; however, epidural administration increased the UA–UV difference. The UA–UV difference at caesarean section was not significantly altered by the onset of labour. There was no correlation between UV pH and UA–UV plasma oxytocin. Cystine aminopeptidase activity was not detectable in UA and UV plasma.Conclusions Fetal OT production is increased by epidural but not by pethidine analgesia. It is not influenced by the onset of labour or fetal hypoxia.

Notes: Objective To determine if erythrocyte sodium pump function is altered with the onset of pregnancy induced hypertension.Design A prospective descriptive study.Subjects Thirty-two primigravid women with pregnancy-induced hypertension (17 had proteinuria) and 32 gestation-matched normotensive primigravid pregnant women were studied and measurements repeated 20 weeks after delivery.Intervention Erythrocyte sodium, ouabain-sensitive sodium flux and the sodium pump rate constant were measured in whole blood and the maximum velocity and sodium affinity of the sodium pump were measured in vitro.Results Blood pressure remained higher after delivery in the women who had been hypertensive during pregnancy. In normal pregnancy erythrocyte sodium was decreased, and ouabain-sensitive sodium flux, the sodium pump rate constant and maximum velocity (Vmax) were increased compared with 20 weeks after delivery. In pregnancy-induced hypertension erythrocyte sodium and sodium pump changes were the same as in normal pregnancy. The possibility of a positive association between changes in erythrocyte sodium and in blood pressure was excluded. The rate constant of the sodium pump in blood was related to its Vmax measured in vitro but the relation had greater variance in the hypertensives with 7 of the 32 women having rate constants greater than expected from their Vmax.Conclusion There was no evidence of sodium pump inhibition or a rise in intracellular sodium associated with increased blood pressure in pregnancy. There may have been stimulation of the sodium pump by a plasma factor in some hypertensive woman.

Notes: Summary. The capacity of the human placenta to degrade 125I-labelled arginine vasopressin (125I-AVP) was studied in vitro using a dual circuit perfused lobule preparation. Seven placentas were perfused with the perfusate on the maternal side of the lobule containing 125I-AVP at the upper limit of the physiological range. On average, over a 30-min period, 48% of the 125I-AVP appeared to have been metabolized. With one exception, a patient whose labour was augmented with intravenous oxytocin, no 125T-AVP apparently crossed the placental lobule to the fetal circulation. These data indicate that the human placenta has a considerable capacity to degrade AVP.

Notes: Summary. Maternal immunosuppression with azathioprine during pregnancy can depress fetal haemopoiesis resulting in neonatal throm-bocytopenia and leucopenia with the potential for serious sequelae. The effect on the infant of adjusting azathioprine dosage on the basis of maternal total leucocyte count has been studied in 10 pregnancies in eight renal allograft recipients. Throughout the first six pregnancies azathioprine dosage was unchanged and although the characteristic pregnancy leucocytosis was evident it was not maintained in four patients whose leucocyte counts by 32 weeks gestation were significantly less than our norm [10·3 (SD 1·7) ×109/1] and who subsequently had babies with cord leucocyte counts 〈inlineGraphic alt="leqslant R: less-than-or-eq, slant" extraInfo="nonStandardEntity" href="urn:x-wiley:14700328:BJO233:les" location="les.gif"/〉8·0×109/l, again significantly less than our norm [13·7 (SD 3·9) ×109/1]. A significant correlation existed between maternal leucocyte counts at 32 weeks gestation and at delivery and cord leucocyte count (r=0·847; P〈0·01 and r=0·915; P〈0·01 respectively). Three of these infants had platelet counts 〈inlineGraphic alt="leqslant R: less-than-or-eq, slant" extraInfo="nonStandardEntity" href="urn:x-wiley:14700328:BJO233:les" location="les.gif"/〉100×109/1 but there was no correlation between maternal platelet counts at 32 weeks gestation or at delivery and cord platelet count. For the next four pregnancies policy changed: at 32 weeks gestation azathioprine dosage was halved if maternal leucocyte count was at or below the ISD band (8·6×109/1) for normal pregnancy. All of the infants were haemotologically normal and two patients whose first babies had leucopenia and thrombocytopenia had second babies without problems. Analysis of data from all 10 pregnancies still demonstrated a significant correlation between cord leucocyte count and maternal leucocyte count at delivery but no longer at 32 weeks gestation. It is concluded that in pregnant renal allograft recipients adjustment of azathioprine dosage so as to maintain maternal total leucocyte count within normal physiological limits for pregnancy avoids neonatal leucopenia and thrombocytopcnia.

Notes: Serial changes in 24-hour creatinine clearance were determined in 11 women during several menstrual cycles before conception, the conceptional cycle and the first trimester of pregnancy. During the menstrual cycle, a 20 per cent mean increase occurred between the week of menstruation and the late luteal phase. Following conception, this increase continued such that a 45 per cent mean increase was evident by the ninth week of gestation. In two women who aborted spontaneously, the change in 24-hour creatinine clearance in early pregnancy was not as great nor as sustained, this feature being apparent at least three weeks before any clinical abnormality. Possible reasons for the changes in glomerular filtration rate in early pregnancy and its clinical implications are discussed.

Notes: Twenty-four women were investigated serially during and after normal pregnancy. Plasma uric acid concentration appeared to be inversely related to uric acid clearance under infusion conditions, and comparison with simultaneous inulin clearance suggested an alteration in renal function resulting in increased ‘net tubular reabsorption’ of uric acid as pregnancy progressed. No difference was detected between primigravidae and multigravidae. The implications of these changes are discussed with reference to the renal handling of uric acid in pre-eclampsia.

Notes: Tubular reabsorption of glucose has been measured during glucose infusion in 29 healthy women during and after pregnancy. All the women had normal glucose tolerance to an oral load, and normal glucose excretion when not pregnant, but exhibited a wide range of daily glucose excretion in pregnancy. Throughout pregnancy the renal reabsorption of glucose is less effective than in the non-pregnant state and, in general, the greater the amount of glycosuria which develops in pregnancy, the less effective is the reabsorption during infusion. Post partum, women with minor degrees of glycosuria during the preceding pregnancy return to a normal highly efficient reabsorption performance during infusion, but women who exhibit greater degrees of glycosuria have a reduced capacity to reabsorb even though they are no longer glycosuric after the pregnancy. It is concluded that pregnancy imposes some specific change in the glucose reabsorptive capacity of the proximal tubule and that women with more than usual degrees of glycosuria in pregnancy may, in addition, have an element of tubular damage. This is discussed in relation to other renal function changes in pregnancy in an attempt to explain the characteristic intermittency of clinical glycosuria in pregnancy.