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Hypoxic-ischemic encephalopathy (HIE) is the result of a chain of events caused mainly by cytokines and nitric oxide (NO) release, which is later on followed by free oxygen radical injury. To investigate NO involvement in asphyxiated newborns, serum and cerebrospinal fluid (CSF) values of NO levels in 17 neonates with HIE were detected. Infants at or above 37 weeks of gestation were classified to have mild, moderate and severe HIE due to Sarnat and Sarnat. Samples obtained between 24 and 72 h of life were immediately frozen at -70 degrees C till the time of measurement by Sievers NOA. Five patients had mild, 6 patients had moderate and 6 patients had severe HIE, 4 in the severe HIE group also had multisystem involvement. The CSF NO levels were significantly higher in moderate and severe HIE groups compared to the mild HIE group (p = 0.028 and p = 0.018 respectively). Our results show that NO level increases in CSF with the severity of HIE between 24 and 72 h following asphyxia. According to the animal work, this is the time period where inducible NO synthase gets activated and could cause neurotoxicity, which might perhaps be prevented by interventions.

While the release of neurotransmitters is involved in the pathophysiology of brain damage following birth asphyxia, it also plays a role in endogenous defense against such damage. Levels of monoamines and the main cerebral monoamine metabolites in the cerebrospinal fluid (CSF) were measured in asphyxiated and control infants within 24 h after birth. The results indicate an increased turnover of noradrenaline (NA) and dopamine following asphyxia. Furthermore, the NA stores in the brain seem to be exhausted in some cases. We conclude that this increase in catecholamine turnover to some extent explains the clinical symptoms of hypoxic-ischemic encephalopathy and that it may reflect an intrinsic adaptive capacity to perinatal distress.