This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Blair, J. L. Articles by Todd, M. M. Search for Related Content PubMed PubMed Citation Articles by Blair, J. L. Articles by Todd, M. M.

Stroke, Vol 20, 507-512, Copyright © 1989 by American Heart Association

ARTICLES

Effects of elevated plasma magnesium versus calcium on cerebral ischemic injury in rats

JL Blair, DS Warner and MM Todd
Department of Anesthesia, University of Iowa, Iowa City 52242.

Both Mg2+ and Ca2+ have been implicated as having roles in the pathomechanisms of cerebral ischemia. To further study the effects of these ions on postischemic histologic outcome, fasted rats were given one of three intravenous infusions: 5.0 mmol/kg MgCl2, 5.0 mmol/kg MgCl2 + 0.035 units/kg regular insulin, or 1.0 mmol/kg CaCl2. This resulted in elevated plasma Mg2+ or Ca2+ concentrations in the corresponding groups. A fourth group received 0.9% NaCl (saline). Preinfusion plasma glucose concentration was similar for all groups and was unchanged after infusion in rats receiving either saline or MgCl2 + insulin. In contrast, postinfusion glucose concentration was increased in the MgCl2 group (p less than 0.001) and decreased in the CaCl2 group (p less than 0.001) relative to saline-treated rats. Following respective infusions, all rats underwent 10 minutes of reversible forebrain ischemia (bilateral carotid artery occlusion and systemic hypotension) followed by 7 days' recovery. Six of 12 CaCl2-treated rats died 2-3 days after ischemia; all other rats remained neurologically indistinguishable, without gross neurologic deficits. Histologic injury in the neocortex and caudate was moderate in all groups. In the hippocampus, MgCl2 + insulin resulted in 66 +/- 6% (mean +/- SD) dead CA1 pyramidal cells, which was similar to the amount in saline-treated rats (68 +/- 10%). Injury was increased in the MgCl2 group (79 +/- 4% dead cells), while in surviving CaCl2-treated rats, injury was decreased (54 +/- 13%). We conclude that the increased injury in MgCl2- treated rats and the decreased injury noted in surviving rats receiving CaCl2 are due to the plasma glucose concentrations present prior to ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				B. Ovbiagele, S. Starkman, P. Teal, P. Lyden, M. Kaste, S. M. Davis, W. Hacke, M. Fierus, J. L. Saver, and on behalf of the VISTA Investigators Serum Calcium as Prognosticator in Ischemic Stroke Stroke, August 1, 2008; 39(8): 2231 - 2236. [Abstract] [Full Text] [PDF]

				T. Razinia, J. L. Saver, D. S. Liebeskind, L. K. Ali, B. Buck, and B. Ovbiagele Body Mass Index and Hospital Discharge Outcomes After Ischemic Stroke Arch Neurol, March 1, 2007; 64(3): 388 - 391. [Abstract] [Full Text] [PDF]

				B. Ovbiagele, D. S. Liebeskind, S. Starkman, N. Sanossian, D. Kim, T. Razinia, and J. L. Saver Are elevated admission calcium levels associated with better outcomes after ischemic stroke? Neurology, July 11, 2006; 67(1): 170 - 173. [Abstract] [Full Text] [PDF]

				K. W. Muir and K. R. Lees Dose Optimization of Intravenous Magnesium Sulfate After Acute Stroke Stroke, May 1, 1998; 29(5): 918 - 923. [Abstract] [Full Text] [PDF]