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Abstract

Cardioprotection by Mg Sulfate (MgSO4) during ischemia/reperfusion (I/R) is attributed largely to the Mg2+ cation. However, Mg-gluconate (MgGl2) may provide added benefit, possibly through its anion's antioxidant properties. Protective effects of both Mg-salts and their anions during 30 min global I and 50 min R were assessed in Langendorff-perfused (Krebs-Henseleit buffer) rat hearts. Recovery of function was compared between untreated hearts and those receiving supplement (2.4 mM MgGl2, MgSO4, or Na2SO4, or 4.8 mM NaGI) for 5 min prior to I and during the initial 30 min R. The final 20 min R was conducted without supplement. End diastolic pressure (EDP, mmHg) of the 50 min reperfused MgGl2 group (2.6) was lower than MgSO4 (16.2) and untreated (35.6) groups, and the NaGI group (25.2) was considerably lower than Na2SO4 (38.8). Recovery of developed pressure (% preischemic DP) at the onset of R for MgGl2 (74.9) was greater than MgSO4 (37.9) and untreated (33.2). After 50 min, MgGl2 (77.9) and MgSO4 (66.9) provided protection compared to untreated (51.8). In separate studies, ESR spin trapping with alpha-phenyl-N-tert-butylnitrone (3 mM PBN) showed that I/R alkoxyl radical production was reduced with MgGl2 (0.0 vs. 2.4 vs. 3.6 mM: 184 vs. 97 vs. 54.8 nM/g tissue x min) to a greater extent than seen with MgSO4 (3.6 mM: 108). Additional studies suggest that Gl(1-), unlike SO4(2-), may scavenge hydroxyl radicals, accounting for the added protection. MgGl2 treated hearts exhibited less postischemic dysfunction and oxidative injury compared to MgSO4, suggesting the contribution of Gl(1-) to cardioprotection.

Plasma-Lyte 148: A clinical review

“…Compared with HCO 3 , lactate or acetate, gluconate exerts little, if any alkalinizing effect[51,72]; therefore its clinical effects in vivo as a metabolically degradable anion appear to be very limited. Gluconate may protect against post ischemic cardiac dysfunction and oxidative injury[73], however there is lack of data on acetate and gluconate levels after PL 148 administration in most surgical settings. In a phase II clinical trial of PL 148 vs a bicarbonate-based cardiopulmonary bypass prime solution, there was a significant increase in unmeasured anions levels after PL 148 administration, which was still present, albeit in smaller concentrations prior to cessation of CPB[74].…”

Citrate treatment reduces endothelial death and inflammation under hyperglycaemic conditions

“…Apart from the chelating capacities of citrates and gluconates, the positive effects of these compounds can originate from their quality as free radical scavengers, 41,42 thereby blocking hyperglycaemia-induced ROS production. 7,32,43 Additionally, citrate is known to maintain the glutathione (GSH)/oxidised glutathione (GSSG) ratio, the central component of the myocardial antioxidant system (reviewed by Mallet et al). 38 …”

Combination ART-Induced Oxidative/Nitrosative Stress, Neurogenic Inflammation and Cardiac Dysfunction in HIV-1 Transgenic (Tg) Rats: Protection by Mg

“…Evidence from our laboratory [31,32,33] and those of others [34,35] suggests that Mg may also exhibit anti-ROS/RNS properties. The protective effects of high Mg 2+ may partially relate to its competitive displacement of low molecular weight iron (pro-oxidant) from membrane phospholipid binding sites, thereby averting site-specific hydroxyl radical formation [31,32,33].…”

“…The protective effects of high Mg 2+ may partially relate to its competitive displacement of low molecular weight iron (pro-oxidant) from membrane phospholipid binding sites, thereby averting site-specific hydroxyl radical formation [31,32,33]. We suggest that both anti-ROS/RNS and anti-calcium properties of Mg may contribute to the protective effects provided by Mg-supplementation against the synergistic oxidative stress and cardiac dysfunction displayed in cART-treated Tg rats.…”