RESUMO
BACKGROUND: Extracorporeal membrane oxygenation (ECMO) has been increasingly applied over recent decades to treat severe cardiogenic shock and acute lung failure and cardiac arrest of various causes. Acute intoxication with therapeutic substances or other chemical substances can cause severe cardiogenic shock or even cardiac arrest. The purpose of this study was to conduct a qualitative systematic review of ECMO use in intoxication and poisoning. METHODS: We searched the PubMed, Medline, and Web of Science databases from January 1971 to December 2021 and selected appropriate studies according to our inclusion and exclusion criteria to evaluate the role of ECMO in intoxication and poisoning systematically. Survival at hospital discharge was examined to describe the outcome. RESULTS: The search resulted in 365 publications after removing duplicates. In total, 190 full-text articles were assessed for eligibility. A total of 145 articles from 1985 to 2021 were examined in our final qualitative analysis. A total of 539 (100%) patients were included (mean age: 30.9 ± 16.6 years), with a distribution of n = 64 (11.9%) cases with venovenous (vv) ECMO, n = 218 (40.4%) cases with venoarterial (va) ECMO, and n = 257 (47.7%) cases with cardiac arrest and extracorporeal cardiopulmonary resuscitation. Survival at hospital discharge was 61.0% for all patients, 68.8% for vaECMO, 75% for vvECMO, and 50.9% for extracorporeal cardiopulmonary resuscitation. CONCLUSION: When used and reported, ECMO seems to be a valid tool for adult and pediatric patients suffering intoxication from various pharmaceutical and nonpharmaceutical substances due to a high survival rate at hospital discharge.
RESUMO
Sirtuin 3 is a nicotinamide adenine dinucleotide dependent mitochondrial deacetylase that governs mitochondrial metabolism and oxidative defense. The demise in myocardial function following myocardial ischemia has been associated with mitochondrial dysfunction. Sirt3 maintains myocardial contractile function and protects from cardiac hypertrophy. The role of Sirt3 in ischemia is controversial. Our objective was to understand, under what circumstances Sirt3 is protective in different facets of ischemia, using an in vitro proof-of-concept approach based on simulated ischemia in cultured cardiomyoblasts. Cultured H9c2 cardiomyoblasts were subjected to hypoxia and/or serum deprivation, the combination of which we refer to as simulated ischemia. Apoptosis, as assessed by Annexin V staining in life-cell imaging and propidium-iodide inclusion in flow cytometry, was enhanced following simulated ischemia. Interestingly, serum deprivation was a stronger trigger of apoptosis than hypoxia. Knockdown of Sirt3 further increased apoptosis upon serum deprivation, whereas no such effect occurred upon additional hypoxia. Similarly, only upon serum deprivation but not upon simulated ischemia, silencing of Sirt3 led to a deterioration of mitochondrial function in extracellular flux analysis. In the absence of oxygen these Sirt3-dependent effects were abolished. These data indicate, that Sirt3-mediated myocardial protection is oxygen-dependent. Thus, mitochondrial respiration takes center-stage in Sirt3-dependent prevention of stress-induced myocardial damage.