Acute Perinatal Hypoxia Impairs Neurobehavioral Development and Increases Basilar Artery Contractility in Adult Male Rats

Adverse effects in early ontogenesis can have a delayed influence on the functioning of various organs. We hypothesized that acute perinatal hypoxia would worsen the neurological status and functioning of cerebral arteries in adult rats. Two-day-old male Wistar rats underwent normobaric hypoxia for 2 h (8% O2 content, «Hypoxia» group), while control rats from the same litters were placed in conditions with 21% O2 content. «Hypoxia» rats exhibited delayed maturation of motor reflexes and reduced learning ability. The levels of key serum biochemical parameters did not differ between the two groups. Contractile responses induced by the thromboxane A2 receptor agonist U46619 were increased in the basilar arteries of the «Hypoxia» group compared to «Control» rats. Endothelium-dependent relaxations to acetylcholine and arterial sensitivity to exogenous NO did not differ between the two groups. The NO-synthase inhibitor increased arterial contractility to a lesser extent in the «Hypoxia» group compared to the «Control» group, which was associated with decreased eNOS protein content in basilar arteries from «Hypoxia» rats. Thus, acute perinatal hypoxia impairs the neurological status of adult male rats, which may be partly associated with decreased blood supply to the brain as a result of weakened anticontractile influence of NO in basilar artery.