Martens H, Schweigel M
Department of Veterinary Physiology, Faculty of Veterinary Medicine, Free University of Berlin, Germany.
Vet Clin North Am Food Anim Pract. 2000 Jul;16(2):339-68. doi: 10.1016/s0749-0720(15)30109-2.
Magnesium is an essential mineral with many physiologic and biochemical functions. Surprisingly, Mg homeostasis is not regulated by a hormonal feedback system, but simply depends on inflow (absorption) from the gastrointestinal tract and outflow (endogenous secretion, requirement for milk production, uptake by tissues). Any surplus (inflow greater than outflow) is excreted via urine. Conversely, if the outflow (mainly milk secretion and endogenous loss) exceeds inflow, hypomagnesemia occurs because of the lack of hormonal mechanisms of homeostasis. The major reason for insufficient inflow is a reduced absorption of Mg from the forestomachs. Recent studies from our laboratory and data from the literature permit the proposal of a putative transport model for the secondary active transport of Mg across the rumen epithelium. This model includes two uptake mechanisms across the luminal membrane (PD-dependent and PD-independent) and basolateral extrusion via a Na/Mg exchange. The well-known negative interaction between ruminal K concentration and Mg absorption can be explained on the basis of this model: an increase of ruminal K depolarizes the potential difference of the luminal membrane, PDa, and as the driving force for PD-dependent (or K-sensitive) Mg uptake. Because Na deficiency causes an increase of K concentration in saliva and ruminal fluid, Na deficiency should be considered a potentially important risk factor. The data obtained from in vitro and in vivo studies on the association of Mg transport, changes of ruminal K concentration, and PDa are extensive and confirm the model, if the ruminal Mg concentrations are below 2 to 3 mM. It is further proposed by the model that the PD-independent Mg uptake mechanism is primarily working at high ruminal Mg concentration (above 2 mM). Mg absorption becomes more and more independent of ruminal K with increasing Mg concentration, which can be considered as an explanation for the well-known prophylaxis of hypomagnesemia by increasing oral Mg intake. Fermentation products, NH4+ and SCFA, influence Mg absorption. The possible meaning regarding the pathogenesis of hypomagnesemia is not quite clear. A sudden increase of ruminal NH4+ should be avoided, because high NH4+ concentrations transiently reduce Mg absorption. The most prominent signs of hypomagnesemia are excitations and muscle cramps, which are closely correlated with the Mg concentration in the CSF. It is suggested that the clinical signs are caused by spontaneous activation of neurons in the CNS at low Mg concentrations, which leads to tetany. Prophylactic measures are discussed in context with the known effects on ruminal Mg absorption.
镁是一种必需矿物质，具有多种生理和生化功能。令人惊讶的是，镁的体内平衡并非由激素反馈系统调节，而是仅取决于胃肠道的流入（吸收）和流出（内源性分泌、产奶需求、组织摄取）。任何多余的部分（流入大于流出）都会通过尿液排出。相反，如果流出量（主要是乳汁分泌和内源性损失）超过流入量，由于缺乏体内平衡的激素机制，就会发生低镁血症。流入不足的主要原因是前胃对镁的吸收减少。我们实验室最近的研究以及文献数据使得能够提出一个关于镁跨瘤胃上皮细胞继发性主动转运的假定转运模型。该模型包括跨腔膜的两种摄取机制（依赖电位差和不依赖电位差）以及通过钠/镁交换进行的基底外侧挤出。瘤胃钾浓度与镁吸收之间众所周知的负相互作用可以基于此模型来解释：瘤胃钾的增加会使腔膜的电位差（PDa）去极化，并作为依赖电位差（或钾敏感）的镁摄取的驱动力。由于钠缺乏会导致唾液和瘤胃液中钾浓度升高，因此钠缺乏应被视为一个潜在的重要风险因素。如果瘤胃镁浓度低于2至3毫摩尔，从体外和体内研究获得的关于镁转运、瘤胃钾浓度变化和PDa之间关联的数据广泛且证实了该模型。该模型还进一步提出，不依赖电位差的镁摄取机制主要在瘤胃镁浓度较高（高于2毫摩尔）时起作用。随着镁浓度的增加，镁的吸收越来越独立于瘤胃钾，这可以被视为通过增加口服镁摄入量来预防低镁血症这一众所周知现象的一种解释。发酵产物、NH4+和短链脂肪酸会影响镁的吸收。其对低镁血症发病机制的可能意义尚不完全清楚。应避免瘤胃NH4+的突然增加，因为高浓度的NH4+会暂时降低镁的吸收。低镁血症最突出的症状是兴奋和肌肉痉挛，这与脑脊液中的镁浓度密切相关。有人认为临床症状是由低镁浓度时中枢神经系统中神经元的自发激活引起的，进而导致手足搐搦。预防性措施结合对瘤胃镁吸收的已知影响进行了讨论。
