pituitrin and Hypoxia-Ischemia--Brain

Hyponatremia, defined by a serum sodium concentration of less than 135 mmmol/l, is a complex clinical occurrence frequently manifested in newborns admitted to the neonatal intensive care unit. The pathogenetic mechanisms and clinical timing underlying the onset of hyponatremia have not been well established in the newborn. Aim of this review is to present a practical approach and management of hypotonic hyponatremia in newborns, with particular emphasis on nephrogenic syndrome of inappropriate antidiuresis, recently described by us for the first time in the literature in a newborn.

Topics: Administration, Oral; Diabetes Insipidus, Nephrogenic; Female; Fluid Therapy; Humans; Hyponatremia; Hypoxia-Ischemia, Brain; Inappropriate ADH Syndrome; Infant; Infant, Newborn; Male; Neurophysins; Polymorphism, Single Nucleotide; Protein Precursors; Syndrome; Urea; Vasopressins

Sensitive biomarkers are needed to rapidly identify high-risk infants after hypoxia-ischemia for neuroprotective treatment. Hypotension is a key determinant of hypoxic-ischemic neural injury, and a potent stimulus of humoral pressors including angiotensin-II and arginine vasopressin. We therefore aimed to quantify the relationship between vasopressin and angiotensin-II levels in the latent phase after hypoxia-ischemia induced by umbilical cord occlusion (UCO) with both the severity of preceding hypotension and subsequent neuronal injury.. Chronically instrumented near-term fetal sheep underwent sham-UCO or UCO for either 15 min or until mean arterial pressure was <8 mmHg. Neuronal injury was assessed after 72 h recovery.. Umbilical cord occlusion was associated with severe hypotension that recovered after UCO; two fetuses developed profound secondary hypotension within 6 h and died. Vasopressin levels but not angiotensin-II were significantly elevated 1-3 h after UCO and were closely associated with the severity of hypotension during UCO and the subsequent severity of neuronal loss in the parasagittal and lateral cortex, caudate nucleus and putamen. The Youden cut-point for vasopressin at 1 h was 180.0 pmol/L, with sensitivity 100% and specificity 92.3% for severe neuronal injury or death.. Vasopressin levels shortly after moderate-severe hypoxia-ischemia may be a useful early biomarker to guide the timely implementation of neuroprotective treatment.. It can be difficuIt to rapidly identify infants who might benefit from therapeutic hypothermia. We investigated whether increases in plasma pressor hormones early after hypoxia-ischemia were biomarkers for neonatal hypoxic-ischemic encephalopathy using near-term fetal sheep. Arginine vasopressin levels were elevated at 1-3 h after hypoxia-ischemia and were predictive of the severity of preceding hypotension and subsequent risk of severe neuronal injury or death after hypoxia-ischemia. Arginine vasopressin may help identify neonates at high risk of hypoxic-ischemic encephalopathy early within the therapeutic window for hypothermia.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Biomarkers; Blood Gas Analysis; Disease Models, Animal; Female; Fetal Hypoxia; Hydrogen-Ion Concentration; Hypotension; Hypoxia-Ischemia, Brain; Male; Nervous System Diseases; Neurons; Sheep; Umbilical Cord; Vasopressins