Postischemic calmodulin gene expression in the rat hippocampus.

The hippocampal calmodulin (CaM) gene expression was determined in the rat after transient forebrain ischemia. Ischemia was induced by the 4-vessel occlusion model, and the hybridized mRNA copy numbers corresponding to the 3 CaM genes detected by phosphorimaging were determined by quantitative in situ hybridization 24 h post-insult. A small, but significant upregulation (by 8.8%) of the CaM I gene was observed in the CA1 pyramidal cell layer, whereas other regions exhibited a maintained or slightly decreased CaM gene expression. The CaM mRNA levels decreased most markedly (by 10-15%) in the hippocampal molecular layers. No consistent correlation was found between the ischemic vulnerability and the CaM gene expression pattern. The results indicate that the induction of delayed neuronal death is not incidental to the transcriptional activation of the CaM genes in the ischemic rat hippocampus in vivo. As the calcium-bound CaM content increases during the ischemic insult, downregulation of the CaM gene expression could be a homeostatic response aimed at maintaining the intracellular level of the active CaM pool.

[Prospective biochemical study of the antioxidant defense capacity in retinopathy of prematurity]. / Az antioxidáns védekezóképesség prospektív, biokémiai vizsgálata retinopathia preamaturorumban.

The study was carried out on 60 oxygen-treated premature infants weighed less than 2000 g (1529 +/- 302 g, x mean +/- S. D.) and on their mothers. Both the Retinopathy of Prematurity screening and the biochemical tests were started at the age of 6 weeks. According to our results, the signs of an acute oxidative stress could be seen in all 60 oxygen-treated prematures erythrocyte's glutathione redox system, independently of the presence of the retinopathy compared to prematures (n = 20) with the same gestational age but without oxygen therapy (1720 +/- 305 g, mean +/- S.D.). The concentrations of free sulfhydril groups in the plasma, and the blood selenium levels were significantly lower in the prematures suffering from moderate retinopathy (n = 5) than in the other oxygen-treated premature without retinopathy (n = 27) and with "any retinopathy" (n = 28) patients groups. The same tendency was seen in the mothers. Vitamin E treatment of "any retinopathy" infants seemed to have a positive effect against the development of Retinopathy of Prematurity. The close correlation found between the antioxidant capacity of the mothers and babies suggest that the supplementation of feeding with sulfur-containing amino acids (methionine, cysteine) during pregnancy would improve the antioxidant capacity of prematures. An antioxidant cocktail (selenium + vitamin E) given to the high-risk mothers (advanced age, smoking, pregnancy-induced hypertension) before delivery as suggested in literature might be useful in prevention of Retinopathy of Prematurity.

Effects of ischemia on cholinergic neurotransmission and electrolyte content in newborn pig lumbar spinal cord.

The biochemical changes of the elements of cholinergic neurotransmission (choline acetyltransferase, ChAT; acetylcholinesterase, AChE; butyrylcholinesterase, BuChE; and muscarinic cholinergic receptors, mAChR) as well as the electrolyte content were studied in ischemic lumbar spinal cord segments of newborn pigs. Ischemia was elicited by ligating the aorta for 30 min. Although no significant changes were observed in the sodium, potassium and calcium content of ischemic spinal cords, the calcium content was slightly elevated, to 119.3% of the control value. Whereas significant depletions were observed in both AChE and ChAT activities (to 69.1 and 87.7% of the control value, respectively), there was no significant change in BuChE activity as compared to the control value. The mAChR were also decreased, from 33.25 +/- 2.2 to 27.18 +/- 1.9 fmol/mg protein, while the Kd value was not significantly altered. It is concluded that even a relatively brief interruption of the oxygen supply can cause severe damage in the lumbar spinal cord of the newborn pig, affecting the cholinergic neurotransmission elements. This animal model might be suitable for studying the effects of hypoxia in newborns and children during chest operations involving the descending aorta.

Effects of ischemia on opioid receptors in newborn pig lumbar spinal cord.

The characteristics of opioid receptors were studied by the binding of (3H)naloxone in ischemic lumbar spinal cord segments of newborn pigs. Ischemia was elicited by ligating the aorta for 30 min. The number of millimicron opioid receptors decreased, from 117 +/- 18 to 89 +/- 11 fmol/mg protein, while the Kd value was not significantly altered. It is concluded that even a relatively brief interruption of the oxygen supply may cause severe damage in the lumbar spinal cord of the newborn pig, affecting the opioid neurotransmission. The animal model employed here might be suitable for studying the effects of hypoxia in newborns and children during chest operations involving the descending aorta.