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* Departments of Physiology and Experimental Medicine and
Medicine, and
Immunochemistry Laboratory, George Washington University Medical Center, Washington, DC 20037
Severe dietary Mg restriction (Mg9, 9% of recommended daily allowance [RDA], plasma Mg = 0.25 mM) induces a pro-inflammatory neurogenic response in rats (substance P [SP]), and the associated increases in oxidative stress in vivo and cardiac susceptibility to ischemia/reperfusion (I/R) injury were previously shown to be attenuated by SP receptor blockade and antioxidant treatment. The present study assessed if less severe dietary Mg restriction modulates the extent of both the neurogenic/oxidative responses in vivo and I/R injury in vitro. Male Sprague-Dawley rats maintained on Mg40 (40% RDA, plasma Mg = 0.6 mM) or Mg100 (100% RDA, plasma Mg = 0.8 mM) diets were assessed for plasma SP levels (CHEM-ELISA) during the first 3 weeks and were compared with the Mg9 group; red blood cell (RBC) glutathione and plasma malondialdehyde levels were compared at 3 weeks in Mg9, Mg20 (plasma Mg = 0.4 mM), Mg40, and Mg100 rats; and 40-min global ischemia/30-min reperfusion hearts from 7-week-old Mg20, Mg40, and Mg100 rats were compared with respect to functional recovery (cardiac work, and diastolic, systolic, and developed pressures), tissue LDH release, and free radical production (ESR spectroscopy and 
-phenyl-N-tert butylnitrone [PBN; 3 mM] spin trapping). The Mg40 diet induced smaller elevations in plasma SP (50% lower) compared with Mg9, but with a nearly identical time course. RBC glutathione and plasma malondialdehyde levels revealed a direct relationship between the severity of oxidative stress and hypomagnesemia. The dominant lipid free radical species detected in all I/R groups was the alkoxyl radical (PBN/alkoxyl: H = 1.93 G, N = 13.63 G); however, Mg40 and Mg20 hearts exhibited 2.7- and 3.9-fold higher alkoxyl levels, 40% and 65% greater LDH release, and lower functional recovery (Mg20 < Mg40) compared with Mg100. Our data suggest that varying dietary Mg intake directly influences the magnitude of the neurogenic/oxidative responses in vivo and the resultant myocardial tolerance to I/R stress.
Key Words: dietary magnesium • substance P • glutathione • malondialdehyde • postischemic heart recovery • postischemic free radicals
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