Short communications

Abstract

Vasopressin in cerebrospinal fluid has been measured in 27 fullterm newborns with hypoxic-ischemic encephalopathy. These newborns were divided into three groups according to the degree of neurological involvement, and they have been compared with a control group of 10 newborns. Determinations of vasopressin in cerebrospinal fluid and plasma were done by RIA. The cerebrospinal fluid vasopressin in asphyxiated newborns was higher than in the control group (p < 0.001); the mean concentration in the group of newborns classified as moderate or severe hypoxic-ischemic encephalopathy was higher than in the control group (18.7 pg/ml vs 4.66 pg/ml), and also higher than in the group classified as mild (14.2 pg/ml). Cerebrospinal fluid vasopressin values have a direct relationship to the plasmatic values at 12 hours of life (r = 0.76; p < 0.001). We concluded that vasopressin values in cerebrospinal fluid at 12 hours increase according to the clinical severity of the neonatal hypoxic-ischemic encephalopathy and that they have a strong relationship with plasmatic vasopressin.

Birth elicits a conserved neuroendocrine response with implications for perinatal osmoregulation and neuronal cell death

“…Copeptin/VP levels in cord blood correlate closely with those in cerebrospinal fluid of human newborns 36,37 , indicating concomitant peripheral and central release. The SCN and PVN are the main contributors of VP in cerebrospinal fluid 38 , and VP is released from the dendrites of magnocellular VP neurons in the rat hypothalamus in an activity-dependent manner 78,79 .…”

“…Vasopressin treatment at birth reduces neuronal cell death in the PVN and AHA. Plasma copeptin/VP levels correlate closely with levels in cerebrospinal fluid in human newborns 36,37 , indicating that birth is associated with concomitant peripheral and central VP release. In rodents, the SCN and PVN are the main source of VP in cerebrospinal fluid 38 , and these regions were highly activated at birth (Fig.…”

Neonatal resuscitation in low-resource settings: What, who, and how to overcome challenges to scale up?

“…Current recommendations for neonatal encephalopathy also include fluid restriction and avoidance of fluid overload to avert cerebral edema [67] and overcome the effect of excessive vasopressin release after intrapartum hypoxia [68,69]. A recent Cochrane review [70] evaluated all randomized or quasi-randomized trials of fluid restriction in term newborns suffering intrapartum-related hypoxia, but found no studies that met the criteria for inclusion.…”

Vasopressin excites interneurons to suppress hippocampal network activity across a broad span of brain maturity at birth

“…During delivery, AVP secretion from the hypothalamic nuclei into the fetal circulation via the posterior pituitary is massively elevated ( 13 – 18 ). In sheep and humans ( 19 – 21 ), this parturition-related AVP surge has been shown to take place both in the blood and cerebrospinal fluid, further suggesting that central and peripheral vasopressinergic pathways are activated in parallel at birth. In the present context, it is of particular interest that hypoxia is an effective trigger of AVP release ( 13 , 14 , 18 , 22 ), and that experimental neonatal asphyxia in the rat activates neurons in the PVN ( 23 ), which have central projections.…”