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Biomedical subjects

J M Davison

Publications and source records attributed to J M Davison.

At least 73 records · Page 4Linked to original sources
PubMed1989

Pre-eclampsia as a multi-system disease.

Pre-eclampsia cannot be defined precisely by clinical signs which are just readily detectable secondary features of the primary abnormality within the uterus. The multisystem sequelae could be thought of as a secondary maternal adaptation, with the large variation in clinical presentation reflecting variable susceptibility of maternal target organs. The changes may be characteristic of pre-eclampsia but are not specific and therefore reflect a process rather than a discrete disease entity. Because the pathogenesis is so controversial it is not surprising that views on management differ so much.

Female↗
PubMed1989

Volume homeostasis and osmoregulation in human pregnancy.

This chapter reviews alterations in volume and sodium homeostasis and osmoregulation during human pregnancy. Pregnant women undergo extracellular and plasma volume increases of 50-70%, and these changes accompany marked cumulative sodium retention shared by both mother and fetus. Pregnancy alters several factors with opposing effects on renal salt handling; however, mechanisms by which gestational sodium accumulation and volume expansion are achieved remain obscure. Furthermore, despite substantial increases in absolute blood volume, considerable uncertainty exists as to how this volume is sensed, particularly in late pregnancy when a rapid increase in volume is associated with decreases in peripheral resistance and blood pressure. Attempts to assess 'effective' intravascular volume suggest that pregnant women sense their volume as normal. Osmoregulation is also changed. Body tonicity and the osmotic thresholds for AVP release and thirst decrease by about 10 mosm/kg. The mechanisms responsible for the osmoregulatory changes are obscure. Haemodynamic stimuli such as decrements in blood pressure and of 'effective circulating volume' do not seem to account for them. Of the many increments in hormone levels known to accompany gestation, only hCG has so far been implicated in these changes. Pregnant women experience three- to fourfold increments in AVP disposal rates between early and mid pregnancy; this may be caused by the striking rise in circulating cystine-aminopeptidase (vasopressinase) which also occurs during this period. The increments in MCR may be one reason why the hormonal response to a given osmotic stimulus appears to decrease in late pregnancy. All these alterations permit speculation on the manner in which the decrease in Posm occurs and is maintained within narrow limits. Lowering the osmotic threshold to drink stimulates a rise in water intake and dilution of body fluids. Since AVP release is not suppressed at the usual level of hypotonicity, AVP continues to circulate at levels sufficient to permit water retention. Posm continues to decline until it decreases below the new osmotic thirst threshold, when a new steady state is established. At this point water turnover, too, resembles that in the non-pregnant state. The change in MCR and the marked increment in plasma vasopressinase may explain certain observations regarding disordered water metabolism during late pregnancy. These are the transient DI syndromes due either to subclinical hypothalamic disease or to a disorder peculiar to pregnancy which is AVP-resistant but dDAVP-responsive; the latter analogue resists degradation by vasopressinase.

Arginine Vasopressin↗
PubMed1989

Amniotomy-induced labour is not mediated by endogenous oxytocin.

A technique for complete oxytocinase inhibition has been combined with a rapid serial sampling strategy to determine the plasma oxytocin concentration in eight women undergoing amniotomy for the induction of labour at term and in eight control women. Amniotomy was not associated with an increase in plasma oxytocin concentration. Furthermore, the concentrations were not increased for 20 min following the procedure. Labour was not established in any patient by the end of the 30-min study period.

Adolescent↗
PubMed1989

Osmoregulation of thirst and vasopressin release in pregnancy.

Osmoregulation is altered in human gestation, body tonicity declining to a nadir early in pregnancy after which a new steady-state plasma osmolality is maintained until term. Development of precise, sensitive, and specific radioimmunoassays for arginine vasopressin (AVP), which permit clearer definitions of functional properties of the osmoregulatory system, have led to a formulation of how these changes occur (both in women as well as in a gravid rat model). The osmotic thresholds for thirst and antidiuretic hormone release each decrease approximately 10 mosmol/kg during the initial weeks of human gestation. Lowering the threshold to drink stimulates increased water intake and dilution of body fluids. Because AVP release is not suppressed at the usual levels of tonicity, it still circulates and water is retained. Osmolality declines until it decreases below the osmotic thirst threshold (situated several mosmol/kg above that for hormone secretion), and a new steady state, with little change in water turnover, is established. The metabolic clearance rate of AVP is also altered, increasing three- to fourfold between gestational week 10 and midtrimester, paralleling the appearance and rapid rise in circulating cystine-aminopeptidase (vasopressinase), an observation that may explain several disorders of water handling that complicate human pregnancy. Finally, mechanisms responsible for the altered osmoregulation are obscure but chorionic gonadotropin may be involved in the changes during human gestation.

Animals↗
PubMed1989

Changes in the metabolic clearance of vasopressin and in plasma vasopressinase throughout human pregnancy.

Metabolic clearance rates (MCR) of arginine vasopressin (AVP) were measured serially in five women starting before conception, during gestational weeks 7-8 (early), 22-24 (middle), and 36-38 (late pregnancy), and again 10-12 wk postpartum. Hormonal disposal rates were determined after water loading to suppress endogenous AVP release using a constant infusion method designed to achieve three different steady-state concentrations of plasma AVP (PAVP) on each test occasion. Dose schedules were altered in mid- and late pregnancy to obtain comparable AVP levels at each stage of the protocol. Prehydration decreased plasma osmolality sufficiently to suppress AVP release, as circulating AVP-neurophysin measured serially in three of the women was undetectable. The MCR of AVP was similar before conception (0.75 +/- 0.31, 0.79 +/- 0.34, and 0.76 +/- 0.28 liters/min at PAVP of 2.6 +/- 1.9, 4.7 +/- 2.4, and 8.3 +/- 3.9 pg/ml), in early pregnancy (0.89 +/- 0.34, 0.97 +/- 0.04, and 0.95 +/- 0.40 liters/min at PAVP of 2.2 +/- 2.1, 3.9 +/- 3.2, and 7.9 +/- 3.4 pg/ml), and postpartum (0.70 +/- 0.21, 0.69 +/- 0.24, and 0.75 +/- 0.20 liters/min at PAVP 3.5 +/- 1.8, 5.1 +/- 3.7, and 9.1 +/- 4.2 pg/ml). Values at mid-pregnancy (2.8 +/- 1.3, 3.0 +/- 1.2, and 2.7 +/- 1.2 liters/min at PAVP 2.3 +/- 2.2, 4.0 +/- 3.6, and 7.7 +/- 3.9 pg/ml) and late pregnancy (3.2 +/- 1.4, 3.3 +/- 1.4, and 2.9 +/- 1.2 liters/min at PAVP 1.9 +/- 2.0, 3.8 +/- 2.6, and 7.4 +/- 4.1 pg/ml) increased 3-4-fold (all P less than 0.01). Plasma vasopressinase, undetectable at 7-8 gestational wk, increased markedly by mid- and slightly more by late gestation. Finally, relationships between PAVP and urine osmolality were similar before, during, and after pregnancy. We conclude that marked increments in the MCR of AVP occur between gestational weeks 7 and 8 and mid-pregnancy, which parallel the period of greatest rise in both trophoblastic mass and plasma vasopressinase. There was no evidence of a renal resistance to AVP during gestation.

Aminopeptidases↗
PubMed1988

Plasma oxytocin during third stage of labour: comparison of natural and active management.

The incidences of postpartum haemorrhage and retained placenta have decreased with the use of synthetic oxytocin and controlled cord traction. Whether such treatment is valuable is open to question because of the lack of clinical and physiological studies. The physiological effects of synthetic oxytocin on plasma concentrations of oxytocin and events during delivery were assessed. Plasma oxytocin concentration was determined in serial samples during the late second stage and throughout the third stage of labour in 25 women. Ten women received combined ergotamine and synthetic oxytocin intramuscularly and 15 were not treated. The geometric mean plasma oxytocin concentration significantly increased in the women given oxytocin when measured before and after delivery of the fetal anterior shoulder (3.1 (SD 2.0) pmol/l before and 15.9 (2.7) pmol/l after). Six of the women who did not receive treatment showed a significant increase in geometric mean plasma oxytocin concentration before and after delivery of the fetal shoulder (3.2 (2.0) pmol/l before and 6.4 (2.0) pmol/l after) and nine did not show an increase (geometric mean 2.4 (3.1) pmol/l before and 2.2 (2.2) pmol/l after). Of these nine women, two had an abnormal third stage of delivery; one woman had a postpartum haemorrhage and one required manual removal of the placenta. As it is impossible to predict which women will show a rise in the plasma concentration of endogenous oxytocin, intramuscular oxytocin should be given routinely.

Female↗
PubMed1988

Degradation of radiolabelled arginine vasopressin (125I-AVP) by the human placenta perfused in vitro.

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 125I-AVP apparently crossed the placental lobule to the fetal circulation. These data indicate that the human placenta has a considerable capacity to degrade AVP.

Adult↗
PubMed1988

Sodium and water reabsorption in the proximal and distal nephron in conscious pregnant rats and third trimester women.

1. Sodium and water reabsorption were determined in virgin controls and rats at 9 and 20 days of pregnancy during a water diuresis induced and maintained by infusion of 2.5% dextrose and in normally hydrated women during the third trimester and again 2-3 months after delivery. 2. Reabsorption from the proximal tubules and distal nephron segments was assessed using the clearance of lithium as a marker of the sodium and water delivery from the proximal tubules to the loops of Henle. 3. Glomerular filtration rate and whole-kidney reabsorption of sodium and water were significantly increased at both stages of pregnancy in rats and late in pregnancy in women when compared to the respective non-pregnant control. Fractional reabsorption was unaltered in pregnant rats but increased in pregnant women. 4. Proximal tubule sodium and water reabsorption were increased in pregnant rats and women; fractional reabsorption was unaltered. 5. Absolute reabsorption of sodium and water in distal nephron segments were increased during pregnancy in both rats and women. Although increases in fractional reabsorption were detected in pregnant women, this was not the case at either stage of gestation in rats.

Absorption↗
PubMed1988

Suppression of AVP release by drinking despite hypertonicity during and after gestation.

Water drinking suppresses arginine vasopressin (AVP) release before changes in tonicity or volume. To further characterize this oropharyngeal neuroendocrine reflex, we took advantage of ongoing studies of osmoregulation in pregnancy as follows: five women studied serially in early (8 +/- 1 wk, mean +/- SD) and late (32 +/- 3 wk) pregnancy and 8-10 wk postpartum were slowly infused with hypertonic saline for 150 min while drinking water to satiety (drinking started at 120 min). Plasma osmolality (Posmol) at 120 min was increased (277 +/- 3 to 291 +/- 2, 280 +/- 6 to 295 +/- 5, and 287 +/- 1 to 307 +/- 1 mosmol/kg in 1st and 3rd trimesters and postpartum; P less than 0.01), accompanied by increments in plasma AVP (PAVP) up to 7 +/- 5, 5 +/- 3, and 8 +/- 3 pg/ml, respectively (P less than 0.01). PAVP declined as soon as drinking began (P less than 0.01 at 5 min), despite maintenance of peak osmolality for another 30 min. Similar events were recorded in three males. Calculation of normal disappearance rates (t1/2) demonstrated that AVP levels decreased more rapidly (P less than 0.01) in the 3rd trimester compared with early pregnancy and postpartum. Two other subjects became nauseated during their 1st trimester and postpartum tests which permitted comparison of nausea and drinking which evoke central reflexes with opposing action on AVP release. PAVP, which had increased markedly (range 17-42 pg/ml; P less than 0.01), was not abolished by drinking. These data demonstrate the potency of the drinking reflex on osmoregulation in pregnant and nonpregnant subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Serial evaluation of vasopressin release and thirst in human pregnancy. Role of human chorionic gonadotrophin in the osmoregulatory changes of gestation.

Serial studies were designed to characterized changes in osmoregulation throughout gestation. Eight women underwent a 2-h infusion of hypertonic saline before conception, during gestational weeks 5-8, 10-12, and 28-33, and then 10-12 wk postpartum. Basal plasma osmolality (Posmol) was already significantly decreased by 5-8 wk (P less than 0.001) and remained 10 mosmol.kg-1 below nonpregnant values throughout pregnancy. The apparent threshold for AVP release (defined as the abscissal intercept of the regression line relating plasma AVP [PAVP] to Posmol) was also decreased significantly throughout gestation, as was the osmotic threshold for thirst (derived from analogue scales relating desire to drink to Posmol). The decrement in osmotic thirst threshold appeared to precede that for AVP release, and consistent with this 24-h urine volumes were significantly greater at 5-8 wk gestation (P less than 0.05). The slopes of each regression equation defining PAVP vs. Posmol (whose r values ranged from 0.79 to 0.99), very reproducible before and after pregnancy, were similar at 5-8 and 10-12 wk, but were markedly reduced in the third trimester (P less than 0.001). These volunteers had randomly undergone an additional infusion before conception (both tests in the luteal phase of the menstrual cycle) when 10,000 IU of human chorionic gonadotrophin (hCG) had been given intramuscularly over a 5-d period. Serum hCG values between 0.2 and 3.3 U.ml-1 were lower than usually seen in pregnancy, but the osmotic thresholds for AVP release and thirst decreased by 3 and 4 mosmol.kg-1, respectively (P less than 0.05). Finally we studied a patient with a molar pregnancy in whom thresholds for hormone release and thirst were both decreased to values resembling normal gestation and remained so for approximately 6 wk postevacuation, only normalizing when hCG had virtually disappeared from her serum. In contrast, thresholds increased within the first two puerperal weeks in two women with normal pregnancies. These data demonstrate (a) osmotic thresholds for both AVP release and thirst decrease within the very first gestational weeks; (b) increment in PAVP per unit increase in Posmol is reduced late in gestation; and (c) hCG may be involved in the osmoregulatory changes of pregnancy.

Adolescent↗
PubMed1987

Kidney function in pregnant women.

In pregnancy, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) increase to levels approximately 50% to 80% above nonpregnant levels. The increments occur shortly after conception and persist throughout the second trimester, with some reduction in late pregnancy. There is no accelerated growth akin to compensatory hypertrophy. The increased excretion of glucose and other nutrients in as well uric acid and protein is related in part to altered tubular function. These changes in renal physiology are so marked that nonpregnant norms cannot be used for the management of pregnant women. Cognizance of all these alterations is essential if kidney problems in pregnancy are to be suspected, detected, and managed correctly.

Creatinine↗
PubMed1987

Water homeostasis and vasopressin release during rodent and human gestation.

Body tonicity decreases during both human and rodent gestation, manifested by a decrease in Posm of approximately 10 mosm/kg. In humans, the decrease in the osmotic threshold for thirst may precede decrements in the arginine vasopressin (AVP) secretory threshold by several weeks, whereas the metabolic clearance rate of AVP appears markedly increased in the third trimester. The cause of these osmoregulatory changes are unclear, since through 1986 we have been unable to implicate placental extracts, estrogens, progesterone, prolactin, angiotensin II, and certain endorphins in the decreased Posm observed during rat pregnancy. Changes also occur in volume-AVP secretory relationships in pregnancy. For instance, the volume-sensing AVP release mechanisms are altered during gestation in Sprague-Dawley rats in such a way that the increased intravascular volume is recognized as normal.

Animals↗
PubMed1987

Renal transplantation and pregnancy.

Renal transplantation is usually accompanied by an improvement in reproductive function. The possibility of conception in women of childbearing age emphasizes the need for counseling, and couples who want a child should be encouraged to discuss all implications, with the advice based on strict guidelines. If a recipient becomes pregnant, she must be monitored as a high-risk patient. Management requires particular attention to BP control, renal function, and all infection, as well as fetal surveillance. Just under 40% of conceptions do not go beyond the first trimester, but of those that do, greater than 90% end successfully. In most patients, renal hemodynamics improve during gestation, but permanent impairment occurs in 15% of pregnancies. Other patients may experience transient deterioration in late pregnancy (with or without proteinuria). Patients have a 30% chance of developing hypertension, preeclampsia, or both. Despite its pelvic location, the transplanted kidney rarely produces dystocia and experiences no apparent mechanical injury during vaginal delivery. Thus, cesarean section should be reserved for obstetric reasons only. Aseptic technique, bacterial prophylaxis even for trivial surgery, and steroid augmentation are necessary. Preterm deliveries occur in 45% to 60%, and intrauterine growth retardation in at least 20%, of gestations. Neonatal complications include respiratory distress syndrome, leukopenia, thrombocytopenia, adrenocortical insufficiency, and infection. No predominant or frequent developmental abnormalities have been described, and data on infancy and childhood are encouraging. Future goals should be to improve prepregnancy assessment criteria, to reassess the rationale and implications of immunosuppression during pregnancy, and to monitor the remote effects of pregnancy on both renal prognosis and the offspring.

Delivery, Obstetric↗
PubMed1987

Renal haemodynamics and tubular function in human pregnancy.

In human pregnancy, effective renal plasma flow and glomerular filtration rate increase to levels 50-80% above non-pregnant values. The increments occur shortly after conception, persist throughout the second trimester and reduce slightly in late pregnancy. The hyperfiltration of pregnancy does not seem to be a potentially damaging process. The increased excretion of glucose and other nutrients, as well as uric acid and protein, is related in part to altered tubular function. Renal physiology is altered so much in pregnancy that non-pregnant norms cannot be used in antenatal care.

Female↗