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R Prado

Publications and source records attributed to R Prado.

61 records · Page 4Linked to original sources
PubMedDate not supplied

Peroxidative damage to cell membranes following cerebral ischemia. A cause of ischemic brain injury?

Definitive evidence of oxygen radical-mediated lipid peroxidation as a cause of tissue injury in the setting of brain ischemia has proven elusive. We review the experimental data from our own and other laboratories on this subject. Spectroscopic detection of the conjugated diene structure, the earliest structural alteration produced by fatty acid radicalization, is an inconstant and highly focal observation in the recirculated ischemic brain. Alterations of lipid-soluble antioxidants offer an indirect indication of possible free radical reactions. Other inferences of lipid peroxidation have derived from studies of selective disappearance of free fatty acids. Recent studies of tissue conjugated diene in two rat models of thrombotic infarction with acute reperfusion yielded inconsistent evidence for lipid peroxidation, and in rats subjected to 25 min of diffuse forebrain ischemia, no evidence of conjugated diene formation was observed during early recirculation. We conclude that evolving parenchymal injury in these settings is unlikely to derive from spectroscopically observable lipid autoxidation.

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Dendritic development in neocortex of infants with early postnatal life undernutrition.

The structure of large pyramidal cells from layer V of the motor cortex of undernourished and well-nourished infants was studied to determine the effects of postnatal nutrition on cortical dendritic development. In undernourished infants, the arborization and span of the basilar dendrites were decreased in comparison to controls. These findings indicated that undernutrition experienced during the first months of postnatal life could affect the growth of pyramidal cells, especially the formation of basilar dendrites.

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PubMedDate not supplied

Increased cerebral blood flow during hypercapnia is not affected by lesion of the nucleus locus ceruleus.

To test the hypothesis that the putative noradrenergic innervation of intraparenchymal cerebral blood vessels from the nucleus locus ceruleus mediates the vasodilatory response to hypercapnia, regional cerebral blood flow was measured by iodo-[14C]antipyrine autoradiography in awake and restrained rats with unilateral 6-hydroxydopamine lesion of the nucleus locus ceruleus and in unlesioned control rats. Hypercapnia, induced by the inhalation of 5% or 8% CO2 in air for 8 minutes caused a 2 to 5-fold increase in regional cerebral blood flow. However, despite a marked reduction of about 90% in cortical norepinephrine levels ipsilateral to the lesion, blood flow to the frontal and parietal cortex, hippocampus, striatum and cerebellum increased to the same extent in ipsilateral and contralateral regions. Thus, lesion of the locus ceruleus and the resultant depletion of endogenous cortical and hippocampal norepinephrine, does not influence the cerebrovascular response to hypercapnia.

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PubMedDate not supplied

Hyperglycemia reduces the extent of cerebral infarction in rats.

Although hyperglycemia is known to exacerbate neuronal injury in the setting of reversible brain ischemia, its effect on irreversible thrombotic infarction is less well understood. In this study, unilateral thrombotic infarction was induced photochemically in the parietal cortex of Wistar rats. Seven days later, brains were perfusion-fixed for light microscopy. Infarct areas were measured by computer-assisted planimetry on multiple coronal sections at 250-micron intervals; these data were integrated to yield infarct volumes. Fasted, normoglycemic rats were compared with hyperglycemic rats that had received 1.2-1.5 ml of 50% dextrose i.p. 15 minutes prior to the induction of infarction. Infarct volume averaged 12.5 +/- 4.0 mm3 (mean +/- SD) in rats (n = 14) with plasma glucose levels of 72-184 mg/dl; this differed statistically from the average volume of 9.3 +/- 3.3 mm3 observed in rats (n = 13) with elevated plasma glucose (range 264-607 mg/dl). Spearman rank correlation analysis confirmed a significant correlation of larger infarct volumes with lower plasma glucose levels. In contrast, rats receiving mannitol i.p. to produce an osmotic load comparable with that of the dextrose-pretreated animals showed larger infarct volumes than saline-treated controls. The small but definite beneficial effect of hyperglycemia in this end-arteriolar thrombotic infarction model is possibly attributable to improved local energy metabolism at the periphery of the lesion during the early period of lesion expansion.

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