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词汇介绍
拓展阅读
解析
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。
概述
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,慢性肾脏疾病,镁的排泄会受到损害。但是,除非增加镁的摄入量,否则高镁血症不是慢性肾脏疾病的主要特征。
可能导致轻度高镁血症的其他情况是糖尿病性酮症酸中毒,肾上腺功能不全,甲状腺功能减退,甲状旁腺功能亢进和锂中毒。
症状和体征
虚弱和恶心;呼吸障碍;换气不足;低血压;低血钙;心律异常和心搏停止;肌腱反射减弱或缺失;头晕;困倦;心律异常和心搏停止是与心脏有关的高镁血症的可能并发症。镁充当生理钙阻滞剂,导致心脏内的电传导异常。
与血清浓度有关的临床后果:反射降低 4.0 mEq/L,> 5.0 mEq/L延长的房室传导;> 10.0 mEq/L完整的心脏传导阻滞;> 13.0 mEq/L 心脏骤停。注意,预防先兆子痫子宫收缩的治疗范围是:4.0-7.0 mEq/L。
诊断方法
正常的镁含量在1.7至2.3 mg/dL之间,高于此水平且高达7 mg/dL的任何物质均可引起轻微症状,包括潮红,恶心和头痛。镁含量在7至12 mg/dL之间会影响心脏和肺部,其含量上限可能会导致极度疲劳和低血压。高于12 mg/dL的水平会导致肌肉麻痹和过度换气。当水平高于15.6 mg/dL时,该状况可能导致昏迷。
治疗
通常可以预防高镁血症,治疗高镁血症的第一步是识别并停止多余镁的来源。在更严重的情况下,可以使用以下治疗方法:静脉注射葡萄糖酸钙,因为钙可以拮抗镁在神经和心脏功能中的作用。高镁血症的明确治疗需要通过以下途径增加肾镁排泄:肾功能正常的情况下静脉注射利尿剂,当肾脏功能受损且患者因高镁血症而出现症状时可进行透析。
预防
有潜在肾脏问题的人有患高镁血症的风险,因为他们的肾脏可能无法排泄足够的镁。因此避免使用含镁的药物有助于预防并发症。这包括一些非处方抗酸剂和泻药。建议医生对任何表现出相关症状的肾脏表现不佳的人进行高镁血症检查。如果早期诊断,通常可以治疗高镁血症。如果肾功能正常,则肾脏可以迅速排泄多余的镁。严重的情况,尤其是如果被诊断得晚,在肾脏受损的患者中更难治疗。但是,透析和静脉补钙可以迅速缓解症状。肾功能不全的老年人发生严重并发症的风险更高。如果确诊患有高镁血症,已经入院的重症患者死亡率较高。
大鼠高镁血症紊乱,无相关性: 十五肽BPC 157 abrogates,L-NAME和L-精氨酸恶化
发表时间:2017-08-25
影响指数:3.8
作者: Maria Medvidovic-Grubisic
期刊:Inflammopharmacol
The beneficial effect of pentadecapeptide BPC 157 (no muscle weakness, markedly counteracted brain lesions, lessened hypermagnesemia, maintained normokalaemia) is common for a lg–ng/kg dose range and is significant, because the same doses used and beneficial effects were previously noted. Furthermore, combined hyperkalaemia/hypermagnesemia consistently appeared along with worsening and then disappeared with amelioration, indicating that clearly attenuated hypermagnesemia/maintained normokalaemia is suggestive that BPC 157 might, here, also counteract the initial event leading to hypermagnesemia. A supportive analogy is the counteraction of magnesium sulfate-induced writhing that also appears rapidly and is quite specific as it is unaffected by anti-inflammatory drugs (including serotonin and histamine receptor antagonists) and is unaccompanied by prostaglandin release. This effect, along with the illustrative evidence, implies all of the counteracting effects mentioned before (i.e., on paralysis, arrhythmias, and hyperkalaemia, and extreme muscle weakness; parasympathetic and neuromuscular blockade; injured muscle). In contrast, with a worsened course, higher hypermagnesemia, and emerging hyperkalaemia, it is likely that both LNAME and L-arginine might adversely affect the same events (and that these could be again opposed by BPC 157). Also, the BPC 157 beneficial effects in rats overdosed with magnesium should be considered with respect to its possible effect on the evidenced Mg2+ homeostasis tightly controlled by maintaining the equilibrium between intestinal Mg2+ absorption and renal Mg2+ excretion/reabsorption and several Mg2+ transporters and channels implicated in Mg2+ absorption and/or re-absorption.
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