Alterations of Mg²⁺ After Hemorrhagic Shock

Hemorrhagic shock is generally characterized by hemodynamic instability with cellular hypoxia and diminishing cellular function, resulting from an imbalance between systemic oxygen delivery and consumption and redistribution of fluid and electrolytes. Magnesium (Mg) is the fourth most abundant cation overall and second most abundant intracellular cation in the body and an essential cofactor for the energy production and cellular metabolism. Data for blood total Mg (tMg; free-ionized, protein-bound, and anion-bound forms) and free Mg²⁺ levels after a traumatic injury are inconsistent and only limited information is available on hemorrhagic effects on free Mg²⁺ as the physiologically active form. The aim of this study was to determine changes in blood Mg²⁺ and tMg after hemorrhage in rats identifying mechanism and origin of the changes in blood Mg²⁺. Hemorrhagic shock produced significant increases in blood Mg²⁺, plasma tMg, Na⁺, K⁺, Cl^-, anion gap, partial pressures of oxygen, glucose, and blood urea nitrogen but significant decreases in RBC tMg, blood Ca²⁺, HCO₃^-, pH, partial pressures of carbon dioxide, hematocrit, hemoglobin, total cholesterol, and plasma/RBC ATP. During hemorrhagic shock, K⁺, anion gap, and BUN showed significant positive correlations with changes in blood Mg²⁺ level, while Ca²⁺, pH, and T-CHO correlated to Mg²⁺ in a negative manner. In conclusion, hemorrhagic shock induced an increase in both blood-free Mg²⁺ and tMg, resulted from Mg²⁺ efflux from metabolic damaged cell with acidosis and ATP depletion.