228 POSTASPHYXIAL GLUCOSE ADMINISTRATION AGGRAVATES HYPER-INSULENISM IN PIGLETS WITH BILATERAL PNEUMOTHORAX

Abstract

Insulin plays a role as a growth factor in the neuronal maturation and it may also have an influence on hypoxic-ischemic brain injuries in newborns. Clinical studies indicated, that hyperinsulinemia with hypoglycemia developed in asphyxiated neonates. Recently, we have also found a severe cerebrospinal fluid (CSF) hyperinsulinism during neonatal asphyxia in piglet. In the present study, we investigated the effect of postasphyxial glucose administration on the insulin levels measured by RIA in the plasma and CSF in newborn pigs. Bilatenl pneumothorax (PTX) was induced in 16 piglets; stages of the disease were baseline (B), critical (C) phase with cardiovascular and metabolic failure (arterial hypotension, bradycardia, hypoxemia, combined acidosis), and a 180-min recovery (R) after cardiopulmonary an I metabolic (i.v. infusion of NaHCO3 for 15 min, 0.5 mM/I, 10 ml/kg b.w.) resuscitation. 6 piglets (group 1) were also given i.v. glucose infusion (1.1 M/I) in the same final volume (10 ml/kg), while the remaining 10 animals (group 2) received no glucose. Insulin level wss increased in C phase compared to that in B in plasma (1018 ± 231 pM/I vs. 438 ± 81 pM/, n=16, p< 0.001, all values are means ± SEM), but it was unchanged in CSF (38 ± 5 pM/I vs., 42 ± 7 pM/I, n= 16, N.S.). A more severe hyperinsulinemia occurred in group 1 than in group 2 during R (3157 ± 738 pM/I vs. 1358 ± 495 pM/I, p<0.001 at 60-min-R; and 2211 ± 442 pM/l vs. 534 ± 245 pM/I, p<0.001, at 180-min-R). CSF hyperinsulinism was also significantly (p < 0.001) increased in group I compared to that in group 2 during R (239 ± 77 pM/l vs. 60 ± 13 pM/l, at 60-min-R; and 249 ± 52 pM/l vs. 164 ± 52 pM/l, at 180-min-R). In conclusion, glucose administration increased the asphyxia-induced hyperinsulinism in plasma and CSF of piglets, which may alter the severity of neonatal hypoxic-ischemic brain injuries.