Magnesium concentrations in the ventricular and lumbar cerebrospinal fluid of hypomagnesaemic cows

Allsop, T. F.; Pauli, J. V.

doi:10.1016/s0034-5288(18)31848-4

Cited by 19 publications

(6 citation statements)

References 10 publications

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“…The deficient nontetanic cows were also apparently unable to maintain CSF magnesium concentrations while they were severely hypomagnesaemic. Allsop and Pauli ( 1985) recorded a progressive decrease in CSF magnesium concentrations for 16 days before hypomagnesaemic tetany was induced in lactating cows fed a low magnesium diet. There were significant relationships between the concentration of magnesium in CSF and its concentrations in aqueous humour and vitreous humour.…”

Section: Discussionmentioning

confidence: 99%

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in cattle

McCoy¹,

Hutchinson²,

Davison³

et al. 2001

Veterinary Record

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Severe hypomagnesaemia and tetany were induced in 10 lactating cows by feeding them semi-synthetic low magnesium diets and the animals were used to study the stability of postmortem markers of hypomagnesaemic tetany. There were significant relationships between the concentrations of magnesium in either cerebrospinal fluid (CSF) or plasma and either aqueous or vitreous humour. The onset of hypomagnesamic tetany was also associated with low magnesium concentrations in plasma, CSF and aqueous and vitreous humour. Magnesium concentrations less than 0.25 mmol/litre in fresh aqueous humour may be indicative of severe hypomagnesaemia and possible tetany in lactating cows, but the concentration of magnesium in aqueous humour was unstable postmortem. The concentration of magnesium in vitreous humour was relatively stable and a concentration of less than 0.55 mmol/litre could be used as a diagnostic marker of tetany in cattle for up to at least 48 hours postmortem, at ambient temperatures typical of Northern Ireland.

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Section: Discussionmentioning

confidence: 99%

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in cattle

McCoy¹,

Hutchinson²,

Davison³

et al. 2001

Veterinary Record

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“…The [Mg 2+ ] of CSF is greater than that of blood [23,24], indicating that Mg 2+ is actively transported from the blood into CSF [17]. The [Mg 2+ ] of ventricular CSF is higher and more sensitive to changes in [Mg 2+ ] of plasma than that of lumber CSF in cow [25]. The alteration of [Mg 2+ ] of CSF correlates with the extracellular [Mg 2+ ] around neurons, which affects neural activities.…”

Section: Magnesium Homeostasis In the Brainmentioning

confidence: 99%

Magnesium Is a Key Player in Neuronal Maturation and Neuropathology

Yamanaka

Shindo

Oka

2019

IJMS

105

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Magnesium (Mg) is the second most abundant cation in mammalian cells, and it is essential for numerous cellular processes including enzymatic reactions, ion channel functions, metabolic cycles, cellular signaling, and DNA/RNA stabilities. Because of the versatile and universal nature of Mg2+, the homeostasis of intracellular Mg2+ is physiologically linked to growth, proliferation, differentiation, energy metabolism, and death of cells. On the cellular and tissue levels, maintaining Mg2+ within optimal levels according to the biological context, such as cell types, developmental stages, extracellular environments, and pathophysiological conditions, is crucial for development, normal functions, and diseases. Hence, Mg2+ is pathologically involved in cancers, diabetes, and neurodegenerative diseases, such as Parkinson’s disease, Alzheimer’s disease, and demyelination. In the research field regarding the roles and mechanisms of Mg2+ regulation, numerous controversies caused by its versatility and complexity still exist. As Mg2+, at least, plays critical roles in neuronal development, healthy normal functions, and diseases, appropriate Mg2+ supplementation exhibits neurotrophic effects in a majority of cases. Hence, the control of Mg2+ homeostasis can be a candidate for therapeutic targets in neuronal diseases. In this review, recent results regarding the roles of intracellular Mg2+ and its regulatory system in determining the cell phenotype, fate, and diseases in the nervous system are summarized, and an overview of the comprehensive roles of Mg2+ is provided.

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“…Interacting dietary factors which are reported to reduce magnesium absorption include potassium and organic acids (Whitaker 1983). Hypomagnesaemic tetany has been reproduced experimentally in cattle (Allsop and Pauli 1985), sheep (L'Estrange and Axford 1964, Suttle and Field 1969) and goats (Hazarika and others 1991) by feeding them low magnesium semi‐synthetic diets either with or without high concentrations of potassium and citric acid. The suggested dietary magnesium requirements range from 0·8 to 1·8 g/kg dry matter (dm) for non‐lactating sheep and from 1·2 to 1·8 g/kg dm for lactating sheep (Anon 1980, nrc 1985).…”

mentioning

confidence: 99%

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in sheep

McCoy¹,

Bingham²,

Hudson³

et al. 2001

Veterinary Record

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Hypomagnesaemic tetany was induced in non-lactating and lactating ewes by feeding them semi-synthetic low magnesium diets containing additional potassium chloride and citric acid. Aqueous and vitreous humour were sampled from one eye at the time of death (fresh) and from the second eye after the head had been stored at ambient temperature for 24 hours (24.hour). There were significant relationships between the concentrations of magnesium in cerebrospinal fluid and plasma and its concentrations in fresh aqueous humour and fresh vitreous humour. Magnesium concentrations of <0.33 mmol/litre in fresh aqueous humour and <0.50 mmol/litre in 24.hour aqueous humour were associated with severe hypomagnesaemia and tetany. However, the concentration of magnesium in aqueous humour is relatively unstable and, unless the time of death was known accurately, its interpretation would be difficult. Magnesium concentrations of <0.60 mmol/litre in fresh vitreous humour and <0.65 mmol/litre in 24-hour vitreous humour were associated with severe hypomagnesaemia and tetany in adult sheep. The concentration of magnesium in vitreous humour was relatively stable for up to 48 hours postmortem.

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Magnesium concentrations in the ventricular and lumbar cerebrospinal fluid of hypomagnesaemic cows

Cited by 19 publications

References 10 publications

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in cattle

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in cattle

Magnesium Is a Key Player in Neuronal Maturation and Neuropathology

Postmortem biochemical markers of experimentally induced hypomagnesaemic tetany in sheep

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