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.
Keywords: ATP depletion; Acidosis; Hemorrhagic shock; Mg2+; Mg2+ efflux; tMg.