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镁和钾对脑血管的相互作用——从中风角度的探讨。现状与新发现综述

Interactions of Mg and K on cerebral vessels--aspects in view of stroke. Review of present status and new findings.

作者信息

Altura B T, Altura B M

出版信息

Magnesium. 1984;3(4-6):195-211.

PMID:6399342
Abstract

Considerable experimental evidence has accumulated to indicate that brain ischemia or stroke-like events will lead to rapid losses of brain potassium, magnesium, ATP, creatine phosphate and glucose. These events are usually followed by an uptake of sodium and calcium ions. Increased uptake or excess Ca2+ uptake in neuronal cells is thought to be the prime cause of neuronal death in the brain. Mg2+ deficiency is known to produce a host of neurological disturbances in man; experimentally, Mg2+ deficiency leads to excess uptake of Ca2+ in the brain. Strokes and transient ischemic attacks also are known to be associated with neurological disturbances and ionic changes in the brain. Stroke patients have been reported to exhibit deficits in serum and CSF [Mg]. Acute Mg or K deficiency can produce cerebrovasospasm, at least experimentally. The lower the extracellular concentration of either Mg2+ or K+, the greater the magnitude of cerebral arterial contraction. These cerebrovascular contractions induced by lowering either the [Mg2+]0 or [K+]0 cannot be antagonized or attenuated by known pharmacologic antagonists. The cerebrovasospasms produced upon lowering [Mg2+]0 can be modulated by [K+]0 and vice versa; e.g. the lower the [K+]0, the greater the degree of vasospasm upon withdrawal of [Mg2+]0 and vice versa. Lowering [Mg2+]0 in situ and in vitro results in increased uptake of Ca2+ in the brain and the cerebral arteries. Cerebrovasospasms induced by substances that are known to be released in the brain on injury, such as prostanoids and serotonin, are relaxed dramatically by addition of [Mg2+]0. Infusions of MgSO4 into the brain via the internal carotid artery produces dose-dependent lowering of systolic and diastolic blood pressure as well as dose-dependent vasodilatation of arterioles (17-30 micron) and venules (18-40 micron) in the cerebral microcirculation, as observed by direct in situ high-resolution TV image-intensification microscopy. In clinical studies, infusion of MgSO4 has been reported to alleviate cerebrovasospasms. Epidemiological evidence is accumulating to suggest that consumption of fruit and vegetables (foodstuffs relatively high in K and Mg, and low in Na) is associated in certain geographic regions with a lower than normal incidence of strokes, particularly that of cerebral hemorrhage. On the basis of such data, and the findings reported herein, we believe one must consider that certain types of cerebrovascular accidents, transient ischemic attacks and 'classical' migraine attacks may be associated with a 'true' Mg deficiency and altered fluxes of K+ ions in the brain and CSF.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

大量实验证据表明,脑缺血或类中风事件会导致脑内钾、镁、三磷酸腺苷(ATP)、磷酸肌酸和葡萄糖迅速流失。这些事件之后通常会伴随钠离子和钙离子的摄取增加。神经元细胞中钙离子摄取增加或过量摄取被认为是脑内神经元死亡的主要原因。已知镁缺乏会在人体产生一系列神经功能紊乱;在实验中,镁缺乏会导致脑内钙离子摄取过量。中风和短暂性脑缺血发作也与脑内神经功能紊乱和离子变化有关。据报道,中风患者血清和脑脊液中的镁含量会出现不足。急性镁或钾缺乏至少在实验中会导致脑血管痉挛。细胞外镁离子或钾离子浓度越低,脑动脉收缩的程度就越大。降低细胞外镁离子浓度([Mg2+]0)或钾离子浓度([K+]0)所引发的这些脑血管收缩,无法被已知的药物拮抗剂拮抗或减弱。降低[Mg2+]0所引发的脑血管痉挛可被[K+]0调节,反之亦然;例如,[K+]0越低,撤去[Mg2+]0时血管痉挛的程度就越大,反之亦然。在体内和体外降低[Mg2+]0会导致脑和脑动脉中钙离子摄取增加。已知在脑损伤时会释放的物质,如前列腺素和血清素,所引发的脑血管痉挛,在添加[Mg2+]0后会显著缓解。通过颈内动脉向脑内注入硫酸镁,会导致收缩压和舒张压呈剂量依赖性降低,以及脑微循环中(17 - 30微米的)小动脉和(18 - 40微米的)小静脉出现剂量依赖性血管舒张,这是通过直接原位高分辨率电视图像增强显微镜观察到的。在临床研究中,据报道注入硫酸镁可缓解脑血管痉挛。越来越多的流行病学证据表明,在某些地理区域,食用水果和蔬菜(钾和镁含量相对较高、钠含量较低的食物)与中风发病率低于正常水平有关,尤其是脑出血。基于这些数据以及本文报道的研究结果,我们认为必须考虑到某些类型的脑血管意外、短暂性脑缺血发作和“典型”偏头痛发作可能与“真正的”镁缺乏以及脑和脑脊液中钾离子通量改变有关。(摘要截选至400字)

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