The effect of continuous treatment with sodium nitroprusside on the serum kinetics of the brain marker protein S-100beta in neonates undergoing corrective cardiac surgery by means of hypothermic cardiopulmonary bypass.
Neonates who undergo cardiac surgery of d-transposition of the great arteries by means of hypothermic cardiopulmonary bypass (CPB) represent a group at increased risk to develop brain injury and altered psychomotor development in early life. Measurement of protein S-100beta, an astrocytic calcium binding protein, in serum may provide information on transient astroglial cell activation and disintegration of the related blood-brain barrier due to oxidative stress during and after CPB. Conflicting results have been reported that concern the neuroprotective effect of the NO liberator sodium nitroprusside (SNP) in vitro. We evaluated the effect of continuous treatment with SNP on the serum kinetics of S-100beta in infants and children after corrective cardiac surgery. The data on 25 neonates treated intraoperatively and postoperatively and 28 without treatment were analyzed. SNP was infused (1-5 microg/kg body weight/minute depending on the haemodynamic status) after the induction of anesthesia, and during and after the termination of CPB for 2 days. Serum concentrations of S-100beta were analyzed by the use of a commercially available immunoluminometric kit (Byk-Sangtec, Dietzenbach, Germany). There were no significant differences in the bypass data between the SNP-treated and non-treated group. In comparison to the pre-bypass values, a similar increase in the concentration of protein S-100beta was found 2 hours after the termination of CPB in the SNP-treated and non-treated neonates, which decreased over the subsequent 48 postoperative hours. However, significantly lower post-bypass serum levels of S-100beta were found in the SNP-treated group after 24 hours (p = 0.0009) and 48 hours (p = 0.04) of treatment. In conclusion, the significant elevation of serum levels of protein S-100beta may indicate increased astroglial cell reactivity and increased passage into the blood stream. Longer-lasting treatment with NO liberator SNP seemed to decrease the release of S-100beta into the blood stream and may have delayed protection on the astroglial cells. The neurological significance of such an observation, however, should be evaluated in further follow-up studies, which need to include additional neurophysiological and neurodevelopmental tests.
Abdul-Khaliq
H
H
Department of Congenital Heart Defects and Pediatric Cardiology, Deutsches Herzzentrum Berlin, Germany. abdul-khaliq@dhzb.de
Schubert
S
S
Fischer
T
T
Böttcher
W
W
Harke
C
C
Alexi-Meskishvili
V
V
Lange
P E
PE
Blasig
I E
IE
D015415:Biomarkers; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism*; D001026:Coronary Artery Bypass; D006801:Humans; D007036:Hypothermia, Induced; D007231:Infant, Newborn; D009414:Nerve Growth Factors; D009599:Nitroprusside / Q000494:pharmacology*; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000097:blood*; D019616:Thoracic Surgical Procedures / Q000379:methods*
D015415:Biomarkers; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D009599:Nitroprusside