Sepsis-like Energy Deficit Is Not Sufficient to Induce Early Muscle Fiber Atrophy and Mitochondrial Dysfunction in a Murine Sepsis Model.

Sepsis-induced myopathy is characterized by muscle fiber atrophy, mitochondrial dysfunction, and worsened outcomes. Whether whole-body energy deficit participates in the early alteration of skeletal muscle metabolism has never been investigated. Three groups were studied: "Sepsis" mice, fed ad libitum with a spontaneous decrease in caloric intake (n = 17), and "Sham" mice fed ad libitum (Sham fed (SF), n = 13) or subjected to pair-feeding (Sham pair fed (SPF), n = 12). Sepsis was induced by the intraperitoneal injection of cecal slurry in resuscitated C57BL6/J mice. The feeding of the SPF mice was restricted according to the food intake of the Sepsis mice. Energy balance was evaluated by indirect calorimetry over 24 h. The tibialis anterior cross-sectional area (TA CSA), mitochondrial function (high-resolution respirometry), and mitochondrial quality control pathways (RTqPCR and Western blot) were assessed 24 h after sepsis induction. The energy balance was positive in the SF group and negative in both the SPF and Sepsis groups. The TA CSA did not differ between the SF and SPF groups, but was reduced by 17% in the Sepsis group compared with the SPF group (p < 0.05). The complex-I-linked respiration in permeabilized soleus fibers was higher in the SPF group than the SF group (p < 0.05) and lower in the Sepsis group than the SPF group (p < 0.01). Pgc1α protein expression increased 3.9-fold in the SPF mice compared with the SF mice (p < 0.05) and remained unchanged in the Sepsis mice compared with the SPF mice; the Pgc1α mRNA expression decreased in the Sepsis compared with the SPF mice (p < 0.05). Thus, the sepsis-like energy deficit did not explain the early sepsis-induced muscle fiber atrophy and mitochondrial dysfunction, but led to specific metabolic adaptations not observed in sepsis.

Extracorporeal Membrane Oxygenation for COVID 2019-Acute Respiratory Distress Syndrome: Comparison between First and Second Waves (Stage 2).

We aimed to compare the outcomes of patients under veno-venous extracorporeal membrane oxygenation (V-V ECMO) for COVID-19-Acute Respiratory Distress Syndrome (CARDS) between the first and the second wave. From 1 March 2020 to 30 November 2020, fifty patients requiring a V-V ECMO support for CARDS were included. Patient demographics, pre-ECMO, and day one, three, and seven on-ECMO data and outcomes were collected. The 90-day mortality was 11% higher during the second wave (18/26 (69%)) compared to the first wave (14/24 (58%) (p = 0.423). During the second wave, all of the patients were given steroids compared to 16.7% during the first wave (p < 0.001). The second wave's patients had been on non-invasive ventilation support for a longer period than in the first wave, with the median time from ICU admission to ECMO implantation being significantly higher (14 (11-20) vs. 7.7 (5-12) days; p < 0.001). Mechanical properties of the lung were worsened in the second wave's CARDS patients before ECMO implantation (median static compliance 20 (16-26) vs. 29 (25-37) mL/cmH2O; p < 0.001) and during ECMO days one, three, and seven. More bacterial co-infections before implantation and under ECMO were documented in the second wave group. Despite a better evidence-driven critical care management, we depicted fewer encouraging outcomes during the second wave.