ABSTRACT. Umbilical blood was collected immediatelyat birth (<30 s) in full-term infants after vaginal deliveries (n = 33) and elective cesarean sections (n = 11). Blood gases, plasma adenosine, hypoxanthine, and catecholamine concentrations were determined. In vaginally born infants the median arterial adenosine concentration was found to be 0.46 pM (range 0.13-2.06) and the venous 0.48 pM (0.09-1.62). These levels were significantly higher ( p < 0.01) than in infants delivered by elective cesarean section; 0.16 pM (0.04-0.42) in the artery and 0.17 FM (0.02-0.56) in the vein. Vaginally born infants showed about a 4-fold higher level of umbilical arterial catecholamines than infants born by elective cesarean section. There was a strong inverse correlation between arterial hypoxanthine concentration and pH (r = -0,81, p < 0.01). It is suggested that increased adenosint: release at vaginal delivery modulates the stress response elicited by the strong catecholamine surge and may furthermore exert protective effects in perinatal asphyxia. (Pediatr Res 26:106-108, 1989) The adenosine metabolite hypoxanthine has been found to be released in high concentrations during perinatal asphyxia and is suggested to be an indicator of the severity of hypoxemia (1-4). During hypoxemia increased hypoxanthine production may also be due to an increased adenine nucleotide degradation in skeletal muscle through the route from inosine monophosphate to inosine (cf. 5). The fetus may, however, sustain short periods of moderate hypoxemia also in normal vaginal delivery during uterine contractions (6). It is at present unclear whether this degree of intermittent physiologic fetal hypoxemia during normal delivery is associated with release of adenosine, hypoxanthine, or other purines. The production and release of adenosine seem also to be closely linked to the balance between substrate supply and demand, and therefore increased formation of adenosine may occur during increased metabolic activity (7).Adenosine is a potent vasodilator (8) and exerts inhibitory influence on metabolic processes such as lipolysis (9). It also effectively counteracts myocardial stimulatory effects of catecholamines (10). Furthermore, adenosine or its analogues have been demonstrated to depress breathing particularly in the neonate (1 1, 12). Thus, enhanced formation of adenosine during fetal hypoxia could theroretically be involved in a physiologic defense against hypoxia through its action on metabolism, respiration, and hemodynamics.

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Catecholamine levels were measured in cord arterial blood from preterm infants. Relatively lower catecholamine levels were found in the preterm infants than in term infants, although no significant correlation was found between noradrenaline and adrenaline levels and either gestational age or birthweight. Significantly higher catecholamine levels were found after labour. Preterm females had significantly higher catecholamine levels than boys after asphyxia and tended also to have higher catecholamine levels without asphyxia, although not significant. Catecholamine levels were also significantly elevated in those infants with a low Apgar score (less than 7 at 5 min) and those who were acidotic (cord arterial pH less than 7.25). A good correlation was found between a low Apgar score and the presence of acidosis.

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.

Breathing response to 12% and 6% O2 in N2 (at isocapnia) was measured in anaesthetized piglets, 1-5 and 19-25 days old, before and after 3 mg kg-1 i.v. naltrexone. The degree of interaction between the anaesthetic and naltrexone was assessed. At the end of each hypoxic trial, arterial blood was sampled for measurements of pH and gas tensions, (Met)enkephalin-Arg6-Phe7, adenosine, noradrenaline and adrenalin. Whereas respiration in older animals was stimulated by hypoxia, young piglets had a biphasic response with a pronounced ventilatory decrease in response to severe hypoxia (6% O2/N2). In young animals there was a greater ventilatory response with naltrexone than without the drug, and the biphasic hypoxic response was ameliorated or reversed by naltrexone. Levels of adrenalin increased and those of encephalin, adenosine and noradrenaline tended to increase during hypoxia in the younger age group. Levels of adenosine showed significant increase when data from both age groups and levels of hypoxia were pooled. Combined with previously reported physiological evidence regarding adenosine in hypoxic depression, we conclude that the present results are compatible with a role of opioid peptides and adenosine in the early postnatal response to hypoxia.