Vasopressin but Not Oxytocin Responds to Birth Stress in Infants

ContextBirth triggers a large fetal neuroendocrine response, which is more pronounced in infants born vaginally than in those born by elective cesarean section (ECS). The two related peptides arginine vasopressin (AVP) and oxytocin (OT) play an essential role in peripheral and central stress adaptation and have a shared receptor mediating their function. Elevated cord blood levels of AVP and its surrogate marker copeptin, the C-terminal part of AVP prohormone, have been found after vaginal delivery (VD) as compared to ECS, while release of OT in response to birth is controversial. Moreover, AVP, copeptin and OT have not yet been measured simultaneously at birth.ObjectiveTo test the hypothesis that AVP but not OT levels are increased in infants arterial umbilical cord blood in response to birth stress and to characterize AVP secretion in direct comparison with plasma copeptin.MethodsIn a prospective single-center cross-sectional study, we recruited healthy women with a singleton pregnancy and more than 36 completed weeks of gestation delivering via VD or ECS (cesarean without prior uterine contractions or rupture of membranes). Arterial umbilical cord blood samples were collected directly after birth, centrifuged immediately and plasma samples were frozen. Concentrations of AVP and OT were determined by radioimmunoassay and that of copeptin by ultrasensitive immunofluorescence assay.ResultsA total of 53 arterial umbilical cord blood samples were collected, n = 29 from VD and n = 24 from ECS. Ten venous blood samples from pregnant women without stress were collected as controls. AVP and copeptin concentrations were significantly higher in the VD group than in the ECS group (both p < 0.001), median (range) AVP 4.78 (2.38–8.66) vs. 2.38 (1.79–3.88) (pmol/L), copeptin 1692 (72.1–4094) vs. 5.78 (3.14–17.97), respectively, (pmol/L). In contrast, there was no difference in OT concentrations (pmol/L) between VD and ECS, 6.00 (2.71–7.69) vs. 6.14 (4.26–9.93), respectively. AVP and copeptin concentrations were closely related (Rs = 0.700, p < 0.001) while OT did not show any correlation to either AVP or copeptin. In linear regression models, vaginal delivery and biochemical stress indicators, base deficit and pH, were independent predictors for both AVP and copeptin. OT was not linked to base deficit or pH.ConclusionVaginal birth causes a profound secretion of AVP and copeptin in infants. Whereas AVP indicates acute stress events, copeptin provides information on cumulative stress events over a longer period. In contrast, fetal OT is unaffected by birth stress. Thus, AVP signaling but not OT mediates birth stress response in infants. This unique hormonal activation in early life may impact neurobehavioral development in whole life.

Perinatal lamb mortality - its investigation, causes and control

Methods of investigating perinatal loss in grazing sheep flocks are reviewed and evaluated. The "wet-dry" method is the simplest method for assessing minimal prevalence, whereas the differences between the numbers of single and twin foetuses present at ultrasonic determination of litter size during pregnancy, and the numbers of single and twin lambs present at lamb-marking, is the most precise. The veterinary investigation of field mortality involves full autopsy of a representative sample of dead lambs, a history of prenatal nutrition, disease and husbandry, as well as a qualitative estimate of weather conditions over the period of lamb collection. Pathological processes may be identified in over 95% of deaths and the specific cause determined in about 75% of deaths. The identification of the specific causes in the remainder of deaths, all classified as the starvation-mismothering-exposure (SME) complex, requires intensive, costly, on-site observation, and physiological and biochemical assessment. The probable causes of these deaths include prenatal physiological handicaps resulting from placental insufficiency, aberrant parent-offspring behaviour, management-induced mismothering, misadventure, inadequate milk supply or teat and udder abnormalities, and cold-induced starvation. The gross pathology and pathophysiology of birth stress and the SME complex, which are associated with at least 80% of mortality, are summarised. Birth injury to the foetal central nervous system, characterised by cranial and spinal meningeal haemorrhage is exclusive to parturient deaths and the SME complex. Observed flock prevalences range from 81% to 100% in parturient deaths, and 20% to 57% in the SME complex. The high total prevalence and experimental evidence, indicate the major causal role of birth stress in the pathogenesis of these entities. Lethal congenital malformations, infections (both congenital and acquired after birth), trace element deficiencies and predation are reviewed as minor causes. The new understanding of the pathogenesis of perinatal lamb mortality, recognises the heritable nature of birth mass, maternal pelvic dimensions, parent-offspring behaviour, and the resistance of neonates to cold. Control measures need to incorporate selection for maternal rearing ability, further refinement of prenatal nutritional management of twin-bearing ewes, disease control, provision of shelter for lambing flocks, and avoidance of husbandry: practices which frustrate innate parent-offspring behaviour. A selection programme is summarised.