Abstract

To examine the effect of changes in the state of magnesium balance on ionized magnesium and ionized calcium in serum and brain tissue of female rats. Forty-two mature rats were used in the study. To induce hypermagnesemia, 12 rats received 270 mg/kg of magnesium sulfate intraperitoneally, followed every 20 minutes for 2 hours with 27 mg/kg magnesium sulfate. Ten control rats received an equal volume of saline. To induce hypomagnesemia, ten rats were placed on a magnesium-deficient diet for 4 (n = 5) or 8 (n = 5) days. Ten control rats were placed on basal diets of equal duration. Following treatment, rats were euthanized and serum and brain tissue were analyzed for ionized magnesium and calcium content. Hypermagnesemia produced a significant increase in serum ionized magnesium (P < .05) and calcium (P < .05). In addition, brain levels of ionized magnesium were significantly increased (P < .05), whereas calcium levels significantly decreased (P < .05) particularly in the hippocampus, parietal cortex, and cerebellum. Hypomagnesemia induced by 4 days on a magnesium-deficient diet led to decreased serum ionized magnesium (P < .01) and total magnesium (P < .05) but did not affect brain magnesium levels. Brain levels remained unaltered even after 8 days of hypomagnesemia. Serum and brain ionized calcium were not affected during peripheral magnesium deficiency. During peripheral magnesium deficiency, brain levels of ionized magnesium and ionized calcium are tightly regulated and appear unaffected. However, central levels of these electrolytes are altered under hypermagnesemic conditions. Thus, magnesium administration may change biologically active portions of magnesium and calcium in the brain.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.