Articles: brain-injuries.
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Sheng Li Ke Xue Jin Zhan · Jul 1999
Review[Neural and hemodynamic mechanisms of neurogenic pulmonary edema].
Acute pulmonary edema has been reported in man and animals with intracranial disorders, head trauma or cerebral compression. In anesthetized rats, cerebral compression produced acute, fulminating and fatal lung injury. ⋯ Pulmonary volume loading was the result of drastic decrease in aortic flow accompanying a decline in pulmonary arterial flow. The acute increase in pulmonary blood volume caused severe rises in pulmonary arterial and venous pressures leading to disruption of lung vessels.
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Journal of neurotrauma · Jul 1999
Sequential changes in glial fibrillary acidic protein and gene expression following parasagittal fluid-percussion brain injury in rats.
This study documents the regional and temporal patterns of glial fibrillary acidic protein (GFAP) RNA and protein expression after parasagittal fluid-percussion (F-P) brain injury (1.7 to 2.2 atm) in male Sprague-Dawley rats. In situ hybridization was conducted in 28 rats with a 35S-labeled antisense riboprobe to GFAP at 0.5, 2, and 6 hours and 1, 3, and 30 days after traumatic brain injury (TBI) or sham procedures. Immunocytochemical staining of GFAP was conducted in 20 rats at 1, 3, 7, and 30 days after TBI or sham procedures. ⋯ At 30 days, GFAP mRNA and protein expression were present within the deeper cortical layers of the lateral somatosensory cortex and lateral thalamus and throughout ipsilateral white matter tracts. These data demonstrate a complex pattern of GFAP mRNA and protein expression within gray and white matter tracts following F-P brain injury. Patterns of GFAP gene expression may be a sensitive molecular marker for evaluating the global response of the brain to focal injury in terms of progressive neurodegenerative as well as regenerative processes.
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Journal of neurotrauma · Jul 1999
Differential effects of traumatic brain injury on vesicular acetylcholine transporter and M2 muscarinic receptor mRNA and protein in rat.
Experimental traumatic brain injury (TBI) produces cholinergic neurotransmission deficits that may contribute to chronic spatial memory deficits. Cholinergic neurotransmission deficits may result from presynaptic alterations in the storage and release of acetylcholine (ACh) or from changes in the receptors for ACh. The vesicular ACh transporter (VAChT) mediates accumulation of ACh into secretory vesicles, and the M2 muscarinic receptor subtype can modulate cholinergic neurotransmission via a presynaptic inhibitory feedback mechanism. ⋯ An increase in VAChT mRNA was also observed. Immunohistochemistry demonstrated a loss of M2; however, there was no significant change in M2 mRNA levels in comparison with sham controls. These changes may represent a compensatory response of cholinergic neurons to increase the efficiency of ACh neurotransmission chronically after TBI through differential transcriptional regulation.
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J. Neurol. Neurosurg. Psychiatr. · Jul 1999
Dysautonomia after traumatic brain injury: a forgotten syndrome?
To better establish the clinical features, natural history, clinical management, and rehabilitation implications of dysautonomia after traumatic brain injury, and to highlight difficulties with previous nomenclature. ⋯ Dysautonomia is a distinct clinical syndrome, associated with severe diffuse axonal injury and preadmission hypoxia. It is associated with a poorer functional outcome; however, both the controls and patients with dysautonomia show a similar magnitude of improvement as measured by changes in FIM scores. It is argued that delayed recognition and treatment of dysautonomia results in a preventable increase in morbidity.
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Eur J Cardiothorac Surg · Jul 1999
Cytokine and S100B levels in paediatric patients undergoing corrective cardiac surgery with or without total circulatory arrest.
Neurological damage following cardiopulmonary bypass (CPB) is difficult to objectively evaluate in infants. In adults, serum elevations of astroglial S100B correlate with proven brain injury independent of operative temperature. The deleterious effects of inflammatory cytokines, generated during CPB, on the brain have not been studied in infants using S100B as a marker for cerebral injury. ⋯ (1) The TCA group have prolonged rises of IL-6, IL-8 and S100B. (2) The TCA group generates significantly lower complement. (3) Astroglial injury, seen after surgery, may, in part, be cytokine mediated.