TY - JOUR
T1 - New markers of neonatal neurology
AU - Gazzolo, Diego
AU - Abella, Raul
AU - Marinoni, Emanuela
AU - Di Iorio, Romolo
AU - Li Volti, Giovanni
AU - Galvano, Fabio
AU - Frigiola, Alessandro
AU - Temporini, Francesca
AU - Moresco, Luca
AU - Colivicchi, Micaela
AU - Sabatini, Miriam
AU - Ricotti, Alberto
AU - Strozzi, Maria Chiara
AU - Crivelli, Sandro
AU - Risso, Francesco Maria
AU - Sannia, Andrea
AU - Florio, Pasquale
PY - 2009
Y1 - 2009
N2 - Hypoxiaischemia HI constitutes the main phenomenon responsible for brainblood barrier permeability modifications leading to cerebral vascular auto-regulation loss in newborns. Hypotension, cerebral ischemia, and reperfusion are the main events involved in vascular auto-regulation loss leading to cell death and tissue damage. Reperfusion could be critical since organ damage, particularly of the brain, may be amplified during this period. An exaggerated activation of vasoactive agents, of calcium mediated effects could be responsible for reperfusion injury R-I, which, in turns, leads to cerebral hemorrhage and damage. These phenomena represent a common repertoire in newborns complicated by perinatal acute or chronic hypoxia treated by risky procedures such as mechanical ventilation, nitric oxide supplementation, brain cooling, and extracorporeal membrane oxygenation ECMO. Despite accurate monitoring, the post-insult period is crucial, as clinical symptoms and standard monitoring parameters may be silent at a time when brain damage is already occurring and the therapeutic window for pharmacological intervention is limited. Therefore, the measurement of circulating biochemical markers of brain damage, such as vasoactive agents and nervous tissue peptides is eagerly awaited in clinical practice to detect high risk newborns. The present review is aimed at investigating the role of biochemical markers such as adrenomedullin, a vasoactive peptide; S100B, a calcium binding protein, activin A, a glycoprotein, in the cascade of events leading to I-R injury in newborns complicated by perinatal asphyxia.
AB - Hypoxiaischemia HI constitutes the main phenomenon responsible for brainblood barrier permeability modifications leading to cerebral vascular auto-regulation loss in newborns. Hypotension, cerebral ischemia, and reperfusion are the main events involved in vascular auto-regulation loss leading to cell death and tissue damage. Reperfusion could be critical since organ damage, particularly of the brain, may be amplified during this period. An exaggerated activation of vasoactive agents, of calcium mediated effects could be responsible for reperfusion injury R-I, which, in turns, leads to cerebral hemorrhage and damage. These phenomena represent a common repertoire in newborns complicated by perinatal acute or chronic hypoxia treated by risky procedures such as mechanical ventilation, nitric oxide supplementation, brain cooling, and extracorporeal membrane oxygenation ECMO. Despite accurate monitoring, the post-insult period is crucial, as clinical symptoms and standard monitoring parameters may be silent at a time when brain damage is already occurring and the therapeutic window for pharmacological intervention is limited. Therefore, the measurement of circulating biochemical markers of brain damage, such as vasoactive agents and nervous tissue peptides is eagerly awaited in clinical practice to detect high risk newborns. The present review is aimed at investigating the role of biochemical markers such as adrenomedullin, a vasoactive peptide; S100B, a calcium binding protein, activin A, a glycoprotein, in the cascade of events leading to I-R injury in newborns complicated by perinatal asphyxia.
KW - Activin A
KW - Adrenomedullin
KW - Brain damage
KW - Newborn
KW - Perinatal asphyxia
KW - S100B
UR - http://www.scopus.com/inward/record.url?scp=70449393953&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=70449393953&partnerID=8YFLogxK
U2 - 10.1080/14767050903181468
DO - 10.1080/14767050903181468
M3 - Article
C2 - 19718579
AN - SCOPUS:70449393953
VL - 22
SP - 57
EP - 61
JO - Journal of Maternal-Fetal and Neonatal Medicine
JF - Journal of Maternal-Fetal and Neonatal Medicine
SN - 1476-7058
IS - SUPPL. 3
ER -