Metabolic acidosis after sodium thiosulfate infusion and the role of hydrogen sulfide.
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ABSTRACT:
SUBMITTER: Hunt GM
PROVIDER: S-EPMC6099024 | biostudies-literature | 2018 Aug
REPOSITORIES: biostudies-literature
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Metabolic acidosis after sodium thiosulfate infusion and the role of hydrogen sulfide.
Hunt Guenola M GM Ryder Hilary F HF
Clinical case reports 20180701 8
Sodium thiosulfate (STS), first-line treatment for calcific uremic arteriolopathy, causes a mild asymptomatic acidosis in many patients. However, severe, life-threatening acidosis out of proportion with the expected acid load of STS may occur, potentially due to metabolism of STS to hydrogen sulfide. ...[more]
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Project description:Therapies to accelerate vascular repair are currently lacking. Pre-clinical studies suggest that hydrogen sulfide (H2S), an endogenous gasotransmitter, promotes angiogenesis. Here, we hypothesized that sodium thiosulfate (STS), a clinically relevant source of H2S, would stimulate angiogenesis and vascular repair. STS stimulated neovascularization in WT and LDLR receptor knockout mice following hindlimb ischemia as evidenced by increased leg perfusion assessed by laser Doppler imaging, and capillary density in the gastrocnemius muscle. STS also promoted VEGF-dependent angiogenesis in matrigel plugs in vivo and in the chorioallantoic membrane of chick embryos. In vitro, STS and NaHS stimulated human umbilical vein endothelial cell (HUVEC) migration and proliferation. Seahorse experiments further revealed that STS inhibited mitochondrial respiration and promoted glycolysis in HUVEC. The effect of STS on migration and proliferation was glycolysis-dependent. STS probably acts through metabolic reprogramming of endothelial cells toward a more proliferative glycolytic state. These findings may hold broad clinical implications for patients suffering from vascular occlusive diseases.
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Project description:Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.
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Project description:Laterite ore is one of the important sources of nickel (Ni). However, it is difficult to liberate Ni from ore structure during reduction roasting. This paper provided an effective way for a robust recovery of Ni from laterite ore by H2 reduction using sodium thiosulfate (Na2S2O3) as a promoter. . It was found that a Ni content of 9.97% and a Ni recovery of 99.24% were achieved with 20 wt% Na2S2O3 at 1,100°C. The promoting mechanism of Na2S2O3 in laterite ore reduction by H2 was also investigated. The thermogravimetric results suggested the formation of Na2Mg2SiO7, Na2SO3, Na2SO4, and S during the pyrolysis of laterite with Na2S2O3, among which the alkali metal salts could destroy the structures of nickel-bearing silicate minerals and hence release Ni, while S could participate in the formation of the low-melting-point eutectic phase of FeS-Fe. The formation of low-melting-point phases were further verified by the morphology analysis, which could improve the aggregation of Ni-Fe particles due to the capillary forces of FeS-Fe as well as the enhanced element migration by the liquid phase of sodium silicates during reduction.
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