The effects of chronic Mg deficiency on the distribution of Mg, Ca, Na, and K in brain, muscle, CSF and plasma.

Update Item Information
Publication Type thesis
School or College College of Pharmacy
Department Pharmacology & Toxicology
Author Woodward, David Lee
Title The effects of chronic Mg deficiency on the distribution of Mg, Ca, Na, and K in brain, muscle, CSF and plasma.
Date 1968-08
Description The relation of Mg to Ca, Na and K was examined during a chronic Mg deficiency. Adults rabbits were fed on of four diets for 18 days at which time brain, muscle, plasma, and CSF were analyzed for total Mg, ca, Na, K and CL as well as for free Mg and Ca. Studies of the kinetics of 28Mg and 45Ca distribution were also conducted on rabbits subjected to similar conditions. The overt signs of Mg deficiency consisted of blanched ears, some alopecia, and changes in the condition of the fur. No evidence of gross changes in excitability was observed. Plasma total and free Mg was reduced while the percent free Mg was unaltered. Plasma Na, K and Ca were unaffected by the treatment. The muscle free and total Mg was unaltered. The muscle free and percent free Ca was increased. Sodium, K and Cl were unchanged. The 28Mg RSA as well as the 45CA RSA of muscle was reduced during chronic Mg deficiency. An analysis of the data suggested that active extrusion of Mg and Ca from cells is reduced by Mg deficiency. The results are compatible with the concept that Mg and Ca may be extruded from the cell by a single mechanism which is regulated by the extracellular [Mg]. Brain free and total Mg was unaltered. The free and percent free Ca in brain also increased. Intracellular Na and Cl of brain were slightly increased while intracellular K was reduced. The changes in Na, K, and Cl may be responsible for the cellular hydration which occurred in brain tissue. Magnesium, Ca, Na K, and Cl of CSF were not changed by the Mg depletion. The 28Mg study suggested that Mg enters the brain tissue from the CSF. Because the CSF is the major source of brain Mg and since the CSF [Mg] was constant throughout the test period, the brain 28Mg RSA ws not altered. The constancy of he CSF [Mg], when considered in conjunction with the electrochemical gradient for Mg between plasma and CSF, can reasonably be explained by the existence of two transport systems located n the choroid plexus probably regulates the CSF [Mg]; the other, located at the ECF-choroid plexus cell interface, removes Mg from the intracellular compartment into the ECF. The second pump appears to be analogous to the Mg transport system located in muscle cells, i.e., it function to maintain a normal intracellular concentration of Mg. The results of studies with 45Ca were compatible with Ca entry into the brain ECF directly from the plasma. The study of 45Ca kinetics of brain did not reveal the mechanism responsible for the large increase in the brain intracellular free Ca; however, the evidence suggest that the active extrusion of Ca from the cell is reduced. The results demonstrate that Ca metabolism in interrelated to the metabolism of Mg, while the maintenance of Na and K distribution, in general, appears to be independent in the Mg concentration under the condition of these experiments.
Type Text
Publisher University of Utah
Subject Physiology; Pharmacology
Subject MESH Magnesium; Magnesium Deficiency
Dissertation Institution University of Utah
Dissertation Name PhD
Language eng
Relation is Version of Digital reproduction of "The effects of chronic Mg deficiency on the distribution of Mg, Ca, Na, and K in brain, muscle, CSF and plasma." Spencer S. Eccles Health Sciences Library. Print version of The effects of chronic Mg deficiency on the distribution of Mg, Ca, Na, and K in brain, muscle, CSF and plasma." available at J. Willard Marriott Library Special Collection. QP6.5 1968 .W6.
Rights Management © David Lee Woodward.
Format Medium application/pdf
Identifier us-etd2,10063
Source Original: University of Utah Spencer S. Eccles Health Sciences Library (no longer available).
ARK ark:/87278/s6kw5wjk
Setname ir_etd
ID 192444
Reference URL https://collections.lib.utah.edu/ark:/87278/s6kw5wjk
Back to Search Results