Current neurovascular research
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Stroke is the second leading cause of death worldwide and the number one cause of adult disability in the United States and Europe. A subtype of stroke, subarachnoid hemorrhage (SAH), accounts for 7% of all strokes each year and claims one of the highest mortalities and morbidities. Many therapeutic interventions have been used to treat brain injury following SAH but none have reached the level of effectiveness needed to clinically reduce mortality. ⋯ The results of this study suggest that GRb1 could relieve cerebral vasospasm and potentially provide neuroprotection in SAH victims. The underlying mechanisms may be partly related to inhibition of P53 and Bax dependent proapoptosis pathway. More studies will be needed to confirm these results and determine its potential as a long term agent.
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Near Infrared Spectroscopy (NIRS) is an emerging technique for brain oxygenation monitoring in newborns complicated by acute and chronic hypoxia. However, data regarding cerebral oxygenation normal values are still lacking and matter of debate. Therefore, we investigate whether NIRS parameters in healthy preterm/term infants are gestational age and delivery modalities dependent and correlate with standard monitoring parameters. ⋯ From 34 wks onwards, rSO2 progressively decreased and FTOE increased reaching their lower dip/peak (P<0.001, for all) at 38-39 weeks. rSO2 and FTOE values were significantly different (P<0.05, for both) between preterm and term newborns when corrected for delivery modality. rSO2 correlated (P<0.001 for all) with heart (r=0.63), respiratory (r=-0.58) rate, and with arterial oxygen saturation (r=0.65). In conclusion, in the first 6-hours after birth cerebral oxygenation in healthy newborns is gestational age-dependent and correlated with routine parameters. NIRS reference curve could be particularly useful in sick newborns brain monitoring.
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That promising neuroprotectants failed to demonstrate benefit against stroke highlights the great difficulties to translate preclinical pharmacological effects in clinical outcomes. Part of this hurdle implies the complex response to injury of the neurovascular unit increasing the cerebrovascular permeability at the level of the blood-brain barrier (BBB). Previous studies reported neuroprotection in animal models upon activation of the nuclear receptor PPARalpha(peroxisome proliferator-activated receptor)alpha, but the cellular targets at the BBB level remain largely unexplored. ⋯ Furthermore, co-cultures with ECs from PPAR-alpha-deficient mice revealed that FA had no effect on OGD-induced hyperpermeability. No transcriptional modulation of classical PPAR-alpha target genes such as SOD, ICAM-1, VCAM-1, ACO, CPT-1, PDK-4 or ET-1 was observed in wild type mouse ECs. In conclusion, these results suggest that part of the preventive PPAR-alpha-mediated protection may occur via BBB ECs by limiting hyperpermeability.
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In preterm infants, neurological signs and clinical manifestations of brain damage are limited criteria for diagnosis of neurologic sequelae. Early indicators of brain damage are needed and currently some specific biochemical markers of brain injury are investigated to assess regional brain damage after perinatal asphyxia in neonates. In this study Protein S-100 (PS-100) and Neuron Specific Enolase (NSE) serum levels were studied serially during the perinatal period in preterm neonates with perinatal asphyxia as markers of glial and neuronal damage respectively. ⋯ In neonates with mild asphyxia serum values of both markers showed decreasing levels through the study period. The results of this study suggest that perinatal asphyxia is associated with the release of different brain cellular proteins in the blood of preterm infants with different time course indicating specific regional cellular injury. The more elevated levels of NSE at birth found in the newborns with severe asphyxia could be considered as an early biomarker of neuronal necrotic damage in the ischaemic phase of perinatal cerebral hypoxic-ischaemic insult; progressive increase of PS-100 during the first week of life in the same neonates could be expression of apoptotic damage of glial cells occurring in the reperfusion phase of cerebral ischaemia.
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Spinal cord injury remains a devastating complication of thoracic and thoracoabdominal aortic operations. We aimed to investigate neuro-protective role of melatonin administered to rabbits before ischemia against ischemia-reperfusion (IR) injury. Occlusion of the abdominal aorta was applied to adult rabbits, followed by removal of aortic clamp and reperfusion. ⋯ Histopathologic analyses demonstrated typical morphologic changes characteristic of necrosis in I/R group. Melatonin attenuated ischemia-induced necrosis. Melatonin administration may significantly reduce the incidence of spinal cord injury following temporary aortic occlusion.