Alterations of Mg2+ After Hemorrhagic Shock

Abstract

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 Mg levels after a traumatic injury are inconsistent and only limited information is available on hemorrhagic effects on free Mg as the physiologically active form. The aim of this study was to determine changes in blood Mg and tMg after hemorrhage in rats identifying mechanism and origin of the changes in blood Mg. Hemorrhagic shock produced significant increases in blood Mg, plasma tMg, Na, K, Cl, anion gap, partial pressures of oxygen, glucose, and blood urea nitrogen but significant decreases in RBC tMg, blood Ca, HCO, 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 Mg level, while Ca, pH, and T-CHO correlated to Mg in a negative manner. In conclusion, hemorrhagic shock induced an increase in both blood-free Mg and tMg, resulted from Mg efflux from metabolic damaged cell with acidosis and ATP depletion.

Deficiency of metabolite sensing receptor HCA2 impairs the salutary effect of niacin in hemorrhagic shock

“…Studies from our laboratory and others have demonstrated a significant role for mitochondria in organ dysfunction following hemorrhagic shock [5][6][7]. SIRT1, an NAD + dependent enzyme that catalyses protein deacetylation, is important in the maintenance of mitochondrial function and recent studies showed a declined activity of SIRT1 in animal models of hemorrhagic shock [4,8]. We previously reported that resveratrol and SRT1720, SIRT1 activators, improved survival following hemorrhagic shock [9].…”

“…Despite advances in critical care, severely injured patients still face a high degree of post-injury morbidity and mortality [2]. Hemorrhagic shock is characterized by whole body hypoxia, nutrient deprivation, hemodynamic instability and systemic inflammation, and may lead to multiple organ dysfunction and death [3,4]. Studies from our laboratory and others have demonstrated a significant role for mitochondria in organ dysfunction following hemorrhagic shock [5][6][7].…”

Forensic Medical Aspects of Complications and Lesions of Target Organs with Hemorrhagic Shock

“…Магній (Mg 2+ ) є другим найбільш поширеним внутрішньоклітинним катіоном в організмі і істот-ним кофактором для виробництва енергії і клітин-ного метаболізму. У щурів ГШ викликає підвищен-ня в крові, вільного Mg 2+ і плазматичного tMg 2+ , в результаті виходу Mg 2+ з метаболічно ушкоджених клітини з ацидозом і виснаженим АТФ [9].…”