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Howard Trachtman 《Pediatric nephrology (Berlin, Germany)》1992,6(1):104-112
Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na+)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na+] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema. It is possible that excessive administration of electrolyte-free solutions and high doses of insulin may increase the risk of this complication. While there are some data to suggest that brain cell size is disturbed during acute uremia, additional work is necessary to clarify the role of cerebral cell volume regulation during acute and chronic uremia. 相似文献
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Neurological disorders induced by long-term exposure to organic solvents typically have a slowly progressive clinical course, which may be arrested or even reversed following discontinuation of exposure. We report an unusual case of rapidly progressive toxic leukoencephalomyelopathy in a 29-year-old man who had worked at a chemical factory that used toluene for the manufacture of nylon 66 for 5 years. He presented with progressive weakness of legs, recurrent seizures, and cognitive decline. Widespread white-matter changes in the brain and spinal cord, and myelodysplastic syndrome were noted. He died 6 months after the onset of his symptoms, and autopsy showed discrete multifocal demyelination and necrosis in the central nervous system, and dysplastic cells of erythroid, myeloid, and megakaryotic lineages in blood vessels. The co-occurrence of leukoencephalomyelopathy and myelodysplastic syndrome highlights the vulnerability of the white matter and bone marrow to injury from organic solvents. Intravascular congestion of dysplastic hematopoietic cells might have led to his unusually rapid progression of leukoencephalomyelopathy. 相似文献
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John R. Glowa 《Drug development research》1990,20(4):411-428
Volatile organic solvents exhibit a range of behavioral effects from the insidiously toxic to the beneficial. Solvents impair performance in a concentration-dependent manner that depends on the unique physicochemical properties of each solvent. The toxic effects of solvents range greatly but, at sufficient concentrations, or after prolonged exposure, neurotoxic effects are often seen. Many solvents are both self-administered and exhibit noxious properties. Solvents may produce some of their primary behavioral effects by altering γ-amino-butyric acid (GABA) function. Further studies related to mechanism may lead to a better understanding of means to protect individuals from the effects of solvent exposure, as well as further our knowledge of solvent abuse. Solvents activate the stress axis and, as such, their neuroendocrine effects deserve further characterization, because chronic exposure may result in altered neuronal activity similar to that associated with chronic stress. Methods have been developed to assess for risk of the effects of exposure to solvents, detailing the lowest levels of solvent expected to produce behavioral impairment. Results from these procedures should be applied to the different end points described. 相似文献
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急性有机磷中毒患者的血钾变化及临床意义的探讨 总被引:1,自引:0,他引:1
目的:探讨急性有机磷中毒患的血清钾变化及其临床意义。方法:对68例发病6小时内的急性有机磷中毒的患入院后测定血清钾,并根据不同的中毒程度、中毒方式、发病时间分组在比较,并设正常对照组对照。结果:中毒各组均有明显的低钾血症,与对照组比较均有显性意义(P<0.01),且重度中毒组与中、轻度组比较亦有显性意义(P>0.05),但两种不同的中毒途径与不同的中毒时间的组间血清钾的比较无显性意义(P>0.05)。结论:急性有机磷中毒可致明显的低钾血症,中毒越重,低钾血症越明显。在发病早期应注意监测血清钾的变化,及时纠正低血钾,预防或减轻中毒后严重合并症的产生。 相似文献
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"Chronic painter''s syndrome". A reanalysis of psychological test data in a group of diagnosed cases, based on comparisons with matched controls 总被引:4,自引:0,他引:4
Twenty solvent-exposed workers, most of them painters, had been diagnosed as cases of toxic encephalopathy in 1978/79. Two years later they were re-examined with an extensive battery of neuropsychological tests. Their performance was unchanged on retesting. We have now compared their test results with those of non-exposed control subjects. Previous impressions of significant intellectual impairment in the solvent-exposed patients could not be confirmed when the influence of age, education, and intelligence was taken into consideration. The present group with presumed toxic encephalopathy is assumed to be representative of other patients who were similarly diagnosed in our department. The presently reanalyzed cases had been diagnosed as brain damaged and reported as such in the literature. Thus, they may have contributed to the formation of the concept of the "chronic painters' syndrome" with dementia. 相似文献
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通过电化学共沉积方法制备具有生物活性的有机高聚物/钙磷陶瓷复合膜层。用XPS、SIMS等对复合膜层的化学组分进行表征,证明少量有机高聚物可能在分子层次上掺杂形成有机高聚物/羟基磷灰石复合膜层。对电沉积HAP陶瓷膜层进行微刮痕实验表明,陶瓷膜层与金属基体的结合力得到显著改善。 相似文献