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Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model

Published online by Cambridge University Press:  09 March 2007

Joseph Kurantsin-Mills ,
Marie M. Cassidy ,
Richard E. Stafford  and
William B. Weglicki
Joseph Kurantsin-Mills
Affiliation:
Division of Hematology and Oncology, Department of Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA
Marie M. Cassidy
Affiliation:
Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA
Richard E. Stafford
Affiliation:
Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA
William B. Weglicki
Affiliation:
Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA
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Abstract

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Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-α). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1–2) and chronic phases (week 3–4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.

Keywords

MagnesiumNeutrophiliaInflammatory cells
Type
General Nutrition
Information
British Journal of Nutrition , Volume 78 , Issue 5 , November 1997 , pp. 845 - 855
Copyright
Copyright © The Nutrition Society 1997

References

REFERENCES

Aikawa, J. K. (1981) Magnesium: Its Biologic Significance. Boca Raton, FL: CRC Press.Google Scholar
Altura, B. M. (1986) Magnesium, stress, and the cardiovascular system. Magnesium 5, 103–220.Google Scholar
Baenziger, N. L. & Majerus, P.W. (1974) Isolation of human platelets and platelet surface membranes. Methods in Enzymology 31, 149–155.CrossRefGoogle ScholarPubMed
Battifora, H. (1973). Effect of magnesium deficiency on blood cells: clinical and experimental data. In First International Symposium on Magnesium Deficiency in Human Pathology, pp. 501–515, [Durlach, J. editor]. Paris: ‘Société Générale de l'Eau Minérale, Vittel’ Press.Google Scholar
Bourke, G. J., Daly, L. E. & McGilvaray, J. (1985) Interpretation and Uses of Medical Statistics, 3rd ed. London: Blackwell Scientific Publications.Google Scholar
Bruce, A., Bruce, V., Kurantsin-Mills, J., Cassidy, M. M., Stafford, R. E. & Weglicki, W. B. (1995) Myocardial myeloperoxidase activity and cardiomyopathic injury during magnesium deficiency. FASEB Journal 9, A708.Google Scholar
Dale, D. C. (1992). Neutrophilia. In Hematology, 4th ed., pp. 816–820 [Williams, W. J., Beutler, E., Erslev, A. J. and Lichtman, M. A., editors]. New York, NY: McGraw-Hill Publishing Co.Google Scholar
Donnerer, J. & Amann, R. (1993) The inhibition of neurogenic inflammation. General Pharmacology 24, 519–529.CrossRefGoogle ScholarPubMed
Freedman, A. M., Atrakchi, A. H., Cassidy, M. M., Muesing, R. A. & Weglicki, W. B. (1990 a) Magnesium deficiency-induced cardiomyopathy: protection by vitamin E. Biochemical and Biophysical Research Communications 170, 1102–1106.CrossRefGoogle ScholarPubMed
Freedman, A. M., Cassidy, M. M., Muesing, R. A. & Weglicki, W. B. (1991) Captopril protects against myocardial injury induced by magnesium deficiency. Hypertension (Dallas) 18, 142–147.CrossRefGoogle ScholarPubMed
Freedman, A. M., Mak, I. T., Cassidy, M. M. & Weglicki, W. B. (1990 b) Magnesium deficient red blood cells exhibit an enhanced sensitivity to oxidative stress. Free Radical Biology and Medicine 9, 119.CrossRefGoogle Scholar
Groner, W., Boyett, J., Johnson, A. & Scantlebury, M. (1986) Variability of erythrocyte size and hemoglobin content observed in man and four selected mammals. Blood Cells 12, 65–80.Google ScholarPubMed
Hokfelt, T. (1991) Neuropeptides in perspective: the last ten years. Neuron 7, 867–879.CrossRefGoogle ScholarPubMed
Mills, B. J., Linderman, R. D. & Lang, C. A. (1986) Magnesium deficiency inhibits biosynthesis of blood glutathione and tumor growth in the rat (42260). Proceedings of the Society for Experimental Biology and Medicine 181, 326–332.CrossRefGoogle Scholar
Olivares, R., Ducimetière, P. & Claude, J. R. (1993) Monocyte count: a risk factor for coronary heart disease? American Journal of Epidemiology 137, 49–53.Google Scholar
Phillips, T. M. & Weglicki, W. B. (1994) Elevated tumor necrosis factor (TNFα) levels in the myocardium of Mg-deficient (Mg-Def) rats: inhibition by substance P (SP) receptor blockade. FASEB Journal, 8, A663.Google Scholar
Rishi, M., Ahman, A., Makheja, A., Karcher, D. & Bloom, S. (1990) Effect of reduced dietary magnesium on platelet production and function in hamsters. Laboratory Investigation 63, 717–721.Google ScholarPubMed
Seelig, M. S. (1989) Cardiovascular consequences of magnesium deficiency and loss. American Journal of Cardiology 63, 4G–21G.CrossRefGoogle ScholarPubMed
Seelig, M. S. & Heggtveit, H. A. (1974) Magnesium interrelationships in ischemic heart disease: a review. American Journal of Clinical Nutrition 27, 59–79.CrossRefGoogle ScholarPubMed
Tongyai, S., Rayssiguier, Y., Motta, C., Gueux, E., Maurois, P. & Heaton, F. W. (1989) Mechanism of increased erythrocyte membrane fluidity during magnesium deficiency in weanling rats. American Journal of Physiology 257, C270–C276.CrossRefGoogle ScholarPubMed
Walsh, D. T., Weg, V. B., Williams, T. J. & Nourshargh, S. (1995). Substance P-induced inflammatory responses in guinea pig skin: the effect of specific NK1 receptor antagonists and the role of endogenous mediators. British Journal of Pharmacology 114, 1343–1350.CrossRefGoogle ScholarPubMed
Warren, J. S., Ward, P. A. & Johnson, K. J. (1992). The inflammatory response. In Hematology, 4th ed., pp. 63–70 [Williams, W. J., Beutler, E., Erslev, A. J. and Lichtman, M. A., editors]. New York, NY: McGraw-Hill Publishing Co.Google Scholar
Weglicki, W. B. & Phillips, T. M. (1992) Pathobiology of magnesium deficiency: a cytokine/neurogenic inflammation hypothesis. American Journal of Physiology 263, R734–R737.Google ScholarPubMed
Weglicki, W. B., Stafford, R. E., Freedman, A. M., Cassidy, M. M. & Phillips, T. M. (1993) Modulation of cytokines and myocardial lesions by vitamin E and chloroquine in a Mg-deficient rat model. American Journal of Physiology 264, C723–C736.CrossRefGoogle Scholar