首页 > 内分泌医学词汇大全 > Hypermagnesemia
Hypermagnesemia does not prevent intracranial hypertension and aggravates cerebral hyperperfusion in a rat model of acute hyperammonemia.
高镁血症不能预防颅内高压,并加重急性高镁血症大鼠模型的脑高灌注。

摘要

UNLABELLED:Intravenous infusion of magnesium sulfate prevents seizures in patients with eclampsia and brain edema after traumatic brain injury. Neuroprotection is achieved by controlling cerebral blood flow (CBF), intracranial pressure, neuronal glutamate release, and aquaporin-4 (Aqp4) expression. These factors are also thought to be involved in the development of brain edema in acute liver failure. We wanted to study whether hypermagnesemia prevented development of intracranial hypertension and hyperperfusion in a rat model of portacaval anastomosis (PCA) and acute hyperammonemia. We also studied whether hypermagnesemia had an influence on brain content of glutamate, glutamine, and aquaporin-4 expression. The study consisted of three experiments: The first was a dose-finding study of four different dosing regimens of magnesium sulfate (MgSO4) in healthy rats. The second involved four groups of PCA rats receiving ammonia infusion/vehicle and MgSO4) /saline. The effect of MgSO(4) on mean arterial pressure (MAP), intracranial pressure (ICP), CBF, cerebral glutamate and glutamine, and aquaporin-4 expression was studied. Finally, the effect of MgSO4 on MAP, ICP, and CBF was studied, using two supplementary dosing regimens. In the second experiment, we found that hypermagnesemia and hyperammonemia were associated with a significantly higher CBF (P < 0.05, two-way analysis of variance [ANOVA]). Hypermagnesemia did not lead to a reduction in ICP and did not affect the brain content of glutamate, glutamine, or Aqp-4 expression. In the third experiment, we achieved higher P-Mg but this did not lead to a significant reduction in ICP or CBF.
CONCLUSION:Our results demonstrate that hypermagnesemia does not prevent intracranial hypertension and aggravates cerebral hyperperfusion in rats with PCA and hyperammonemia.

译文

未标记: 静脉输注硫酸镁可预防脑外伤后子痫和脑水肿患者的癫痫发作。神经保护作用是通过控制脑血流量 (CBF) 、颅内压、神经元谷氨酸释放,aquaporin-4 (Aqp4) 表达的影响。这些因素也被认为是参与脑急性肝功能衰竭。我们想研究在门腔吻合术 (PCA) 和急性高血氨血症的大鼠模型中,高血氨血症是否能阻止颅内高压和高灌注的发展。我们还研究了高镁血症是否对大脑中谷氨酸、谷氨酰胺和 aquaporin-4 表达的含量有影响。该研究包括三个实验: 一是调查研究的四个不同的给药剂量硫酸镁治疗方案 (MgSO4) 的健康影响。第二个涉及四组大鼠 PCA 接受氨浸液/车辆和 MgSO4)/盐水。硫酸镁的效果 (月) 的平均动脉压 (MAP) 、颅内压 (ICP),脑血流量、脑组织谷氨酸和谷氨酰胺,和 aquaporin-4 表达进行了研究。最后,对 MgSO4 上图,ICP,脑血流量的影响,使用两个补充加液法。在第二次试验中,我们发现血镁过多和血氨过多有关,与较高的脑血流量 (P <0.05,双因素方差分析【阿诺瓦】)。血镁过多并没有减少谷氨酸含量比较并没有影响到大脑,谷氨酰胺或 Aqp-4 表达。在第三个实验,我们实现了较高的 P-Mg,但这并未导致 ICP 或 CBF 明显减少。
结论: 我们的研究结果表明,血镁过多不防颅内压增高、加重脑 hyperperfusion 大鼠 PCA 和血氨过多。

Hypermagnesemia

内分泌 电解质紊乱 疾病
概述  :  

高镁血症是一种电解质紊乱,血液中的镁含量很高。症状包括虚弱,神志不清,呼吸频率降低和反射减弱,并发症可能包括低血压和心脏骤停。它通常是由肾衰竭引起的,或者是采用诸如含镁的抗酸剂的治疗引起的。不太常见的原因包括肿瘤溶解综合征,癫痫发作和长时间的缺血。原因镁的状态取决于三个器官:肠道中的摄取,骨骼中的储存和肾脏中的排泄。因此,高镁血症通常是由于这些器官(主要是肠道或肾脏)的问题引起的。溶血,红细胞中的镁浓度大约是血清中的三倍,因此溶血会增加血浆中的镁。肌酐清除率低于30 ml/min 时,慢性肾

Hypermagnesemia

释    义   n. 高镁血症

例    句   There is no hypermagnesemia with apparent clinical effect by these doses of magnesium sulfate during operation. 应用本实验剂量的硫酸镁不会造成有临床效应的高镁血症。

请扫描右侧二维码,免费查看词汇专业知识背景