No abstract

The carbon dioxide/bicarbonate (CO2/HCO3−) pair is the main biological pH buffer. However, its influence on biological processes, and in particular redox processes, is still poorly explored. Here we study the effect of CO2/HCO3− on ischemic injury in three distinct models (cardiac HL-1 cells, perfused rat heart and C. elegans). We found that, while different concentrations of CO2/HCO3− do not affect function under basal conditions, ischemia-reperfusion or similar insults in the presence of higher CO2/HCO3− resulted in greater functional loss associated with higher oxidative damage in all models. Since the effect of CO2/HCO3− was observed in all models tested, we believe this buffer is an important determinant of oxidative damage following ischemia-reperfusion.

Background: Aneurysmal subarachnoid hemorrhage (aSAH) is a severe disease, with systemic involvement and complex diagnosis and treatment. Since the current guidelines were published by the AHA/ASA, Neurocritical Care Society and the European Stroke Organization in 2012-2013,there has been an evolution in the comprehension of SAH-associated brain injury and its multiple underlying mechanisms. As a result, several clinical and translational trials were developed or are underway. Objective: The aim of this article is to review some updates in the diagnosis and treatment of neurological complications of SAH. Methods: A review of PubMed (May, 2010 to February, 2022) was performed. Data was summarized. Results: Content of five meta-analyses, nine review articles and 23 new clinical trials, including pilots, were summarized. Conclusions:Advances in the comprehension of pathophysiology and improvements in critical care have been reflected in the reduction of mortality in SAH. However, despite the number of publications, the only treatments shown to be effective in adequate, well-controlled clinical trials are nimodipine and repair of the ruptured aneurysm. Thus, doubts about the optimal management of SAH still persist.

Introduction: Neurocritical care (NCC) education involves integrating knowledge and skills from various complex areas. While the United States of America and Europe regulate didactic core training for medical residencies and fellowships, the quantity and the quality of such training in Brazil remain unclear. Objectives: To understand how NCC training is currently performed in Neurology, Neurosurgery and Intensive Care residencies in Brazil. Methods: A virtual survey was developed with 27 questions about the existence, duration, teaching method, quality of supervision and skills required in NCC training during medical residency. The planned sample was 390 answers. Results: 120 participants from 41 Institutions and 8 Brazilian states replied. Median age was 36 years (26–76 years). About 66% were neurologists and 25% intensivists. Of them, 57% had training in NCC, 65% as mandatory rotation, 60% lasting more than 4 weeks, predominantly in the first 2 years of the course (42 and 45% respectively). Training happened in general Intensive Care Units (48%) with 5–20 beds (65%) under the supervision of intensivists (66%). The methodology most used was bedside discussion (98%). Among procedures skills, more than 80% reported having performed central venous catheter insertion, orotracheal intubation and neuroimaging discussion. The least performed skills were transcranial doppler (21%), electroencephalogram interpretation (20%), neurological multimodal monitoring (25%). It was highlighted that after training, few participants feel comfortable with the following diagnoses: control of intracranial hypertension (48%), spinal cord injury (39%), care for potential donors (42%), post cardiac arrest care (52%). Conclusion: NCC education in Brazil is currently heterogeneous and at an early stage of development. Further studies are necessary to identify areas in need of improvement and promote advancements in the field.

The carbon dioxide/bicarbonate (CO 2 /HCO 3 −) pair is the main biological pH buffer. However, its influence on biological processes, and in particular redox processes, is still poorly explored. Here we study the effect of CO 2 /HCO 3 − on ischemic injury in three distinct models (cardiac HL-1 cells, perfused rat heart and C. elegans). We found that, while different concentrations of CO 2 /HCO 3 − do not affect function under basal conditions, ischemia-reperfusion or similar insults in the presence of higher CO 2 /HCO 3 − resulted in greater functional loss associated with higher oxidative damage in all models. Since the effect of CO 2 /HCO 3 − was observed in all models tested, we believe this buffer is an important determinant of oxidative damage following ischemiareperfusion.