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Effects of reduced dietary magnesium on platelet production and function in hamsters
1Department of Pathology, School of Medicine, George Washington University, Washington, D.C.
Abstract:
The increased vulnerability of animals fed a magnesium (Mg)-deficient (MD) diet to ischemia-induced myocardial necrosis has been attributed to changes in myocardial electrolyte metabolism. However, a variety of hematologic changes have also been reported in MD and some of these, such as an increase in platelet aggregability, may contribute to the increased myocardial vulnerability. In the present study, we quantified the effect of MD on platelet and megakaryocyte abundance as well as on platelet aggregability with and without an administered calcium channel blocker (nifedipine). Hamsters were fed either a "minimal Mg" diet, in which the level of Mg was kept just high enough to prevent seizures, or a "preset Mg" diet containing precisely known amounts of Mg. Animals fed the minimum Mg diet showed an initial increase in the platelet count, which returned to control range when the dietary Mg was increased to 9 mmoles/kg. Animals on the preset Mg diet showed an increased platelet count if the Mg level was 10 mmoles/kg or less. In addition to the increase in number, platelets from MD animals were less responsive to the aggregation-inhibiting effect of nifedipine than were platelets from control animals, although MD itself did not result in an increased aggregability under the conditions used here. Animals with an increase in circulating platelets showed decreased megakaryocyte abundance in the femoral marrow, but megakaryocytes that were present were larger than those in control animals. These results indicate a profound effect of dietary Mg deficiency on platelet biology. The observed changes could contribute to the increase in myocardial vulnerability to injury found in MD animals.
Insights
Magnesium deficiency (MD) in hamsters alters platelet production and function, increasing platelet counts and affecting their response to medication. These hematologic changes may explain heightened heart vulnerability in MD animals.
Area of Science:
- Hematology
- Cardiovascular Physiology
- Nutritional Science
Background:
- Magnesium deficiency (MD) increases susceptibility to ischemia-induced myocardial necrosis.
- Hematologic changes, including platelet hyperaggregability, are implicated in MD-related cardiac vulnerability.
- The precise impact of MD on platelet and megakaryocyte biology requires further elucidation.
Purpose of the Study:
- To quantify the effects of MD on platelet and megakaryocyte abundance.
- To assess platelet aggregability in MD hamsters, with and without nifedipine.
- To investigate the relationship between MD, platelet dynamics, and megakaryocyte changes.
Main Methods:
- Hamsters were fed either a minimal magnesium (Mg) diet or a preset Mg diet.
- Platelet counts and aggregability were measured.
- Megakaryocyte abundance and morphology in femoral marrow were assessed.
- Platelet response to the calcium channel blocker nifedipine was evaluated.
Main Results:
- MD led to an initial increase in platelet count, normalizing with adequate Mg intake (9 mmoles/kg).
- Platelets from MD animals showed reduced responsiveness to nifedipine's aggregation-inhibiting effects.
- MD animals exhibited decreased femoral marrow megakaryocyte abundance but larger megakaryocytes.
- Increased circulating platelets correlated with decreased megakaryocyte numbers in the marrow.
Conclusions:
- Dietary magnesium deficiency profoundly impacts platelet biology, affecting platelet production and function.
- Observed hematologic alterations in MD may contribute to increased myocardial vulnerability to injury.
- MD-induced changes in platelet dynamics warrant further investigation in the context of cardiovascular health.