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Hypoxia experienced by the fetus is beli ved to be a major cause of disturbed CNS function during childhood. During perinatal hypoxia endogenous opioids are released in large amounts and the developing brain in the last week of gestation may be influenced by circulating opioids, down-regulates n-opioid receptors in neonatal brain. The opioid antagonist, Naltrexone (N) blocks opiate receptors in the brain after chronic administration and can result in either up- or down-regulation of opioid receptors in the brain structures. To test the hypothesis that Naltrexone prevents prenatal chronic hypoxia-induced changes in (i-opioid receptor system in developing brain, we quantified optical density of the (i-opioid receptors in several areas of newborn rat brain. In CPu and ZG cerebral structures of rats long-lasting anoxia leads to the decrease in optical density of ^-opioid receptors. Naltrexone prevents optical density of ^-opioid receptors in CPu, OT, MMPoA and LMPoA structures from decreasing.
Among chickens, meat-producing broiler strains are highly prone to develop severe pulmonary hypertension (PH) that is accompanied by endothelial dysfunction in the conduit extrapulmonary arteries. We hypothesized that exposure to chronic prenatal mild hypoxia would accelerate PH and endothelial dysfunction in smaller intrapulpulmonary arteries from broiler chickens. Fertilized broiler and layer (White Leghorn, WL) eggs were incubated under normoxic or hypoxic conditions. Endothelium-dependent (tested with acetylcholine, ACh ) and -independent (tested with sodium nitroprusside, SNP) relaxations of the caudomedial intrapulmonary artery were studied on fetal day 19 and at 2 weeks post-hatch. The response to acute hypoxia in vitro was also studied in the 2 wk-old vessels. Relaxations induced by ACh and SNP were similar in broiler and layer chickens and were unaffected by chronic mild hypoxia during incubation. However, during in vitro acute hypoxia the broiler arteries showed a markedly enhanced contraction. Chronic prenatal hypoxia did not affect the response of intrapulmonary arteries to acute hypoxia. We conclude that early endothelial dysfunction is not present in the small pulmonary arteries of fast-growing broilers after incubation under normoxic or hypoxic conditions. The higher susceptibility of the broiler pulmonary arteries to acute hypoxia might, at least partially, explain the higher susceptibility to PH.
Hypoxia induces an elevation of excitotoxic amino acid concentrations and may influence hypoxic-in- duced basal ganglia injury. During pregnancy, hypoxia as the destructive factor of CNS alters concentration and mental retardation during childhood. The NMDA antagonist, MK-801, is known to block the effect of amino acids and protect the developing brain against hypoxic insults. To test the hypothesis that MK-801 change prenatal hypoxia affects on the optical density of the μ-opioid receptor system in the developing brain, we quantified optical density of the μ-opioid receptors in several areas of newborn rat brain. In the analysed cerebral structures of rats' brains short-lasting hypoxia leads to the decrease in optical density of n-opioid receptors. MK-801 lessens optical density of μ-opioid receptors in CPu, NA and LMPoA structures.
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