The post-asphyxia increase in blood brain barrier acid extrusion was inhibited by systemically administered pharmacological blockers of Na/H exchange, which notably, also abolished post-asphyxia seizures.
A finding of crucial importance here is that the application of MIA completely suppressed the post-asphyxia increase in brain extracellular pH (P = 0.004, n = 5; Fig. 2B).
The parallel post-asphyxia increase in extra- and intracellular pH levels indicated a net loss of acid equivalents from brain tissue that was not attributable to a disruption of the blood brain barrier, as demonstrated by a lack of increased sodium fluorescein extravasation into the brain, and by the electrophysiological characteristics of the blood brain barrier.
Furthermore, if the post-asphyxia increase in intracellular pH would be caused by enhanced neuronal Na/H exchange (or by any acid extruder), this would lead to a simultaneous decrease in extracellular pH (Siesjö, 1985; Chesler and Kaila, 1992; Chesler, 2003) while the opposite was observed.
Infants who were very large for GA (very LGA; above the 97th percentile) had more than a tripled increase in risk of death by asphyxia and malignant neoplasms.
These findings predict that an increase in the severity of birth asphyxia in human newborns is associated with a progressively slower recovery of blood pH that might even include a transient acid shift.
Results indicate that potassium induced a slight, significant increase and asphyxia induced a very large, significant increase in adenosine levels in perilymph effluent.
Concentrations of VEGF were increased in infants with asphyxia when compared to controls (P ⩽ 0.001).
In contrast, in 57 5-year-old children who were at risk for CVI due to pre-maturity or birth asphyxia, a significant increase in the frequency of impairment was seen on six L94 tasks (range 12 38%).
But after severe asphyxia, there was no increase in cytochrome c release and subsequently, caspase-3 and -9 showed no activation if lambs were treated with propofol, suggesting less to no induction of the mitochondrial apoptotic pathway.
