Impact of hyperoxia on the gut during critical illnesses.

Molecular oxygen is typically delivered to patients via oxygen inhalation or extracorporeal membrane oxygenation (ECMO), potentially resulting in systemic hyperoxia from liberal oxygen inhalation or localized hyperoxia in the lower body from peripheral venoarterial (VA) ECMO. Consequently, this exposes the gastrointestinal tract to excessive oxygen levels. Hyperoxia can trigger organ damage due to the overproduction of reactive oxygen species and is associated with increased mortality. The gut and gut microbiome play pivotal roles in critical illnesses and even small variations in oxygen levels can have a dramatic influence on the physiology and ecology of gut microbes. Here, we reviewed the emerging preclinical evidence which highlights how excessive inhaled oxygen can provoke diffuse villous damage, barrier dysfunction in the gut, and gut dysbiosis. The hallmark of this dysbiosis includes the expansion of oxygen-tolerant pathogens (e.g., Enterobacteriaceae) and the depletion of beneficial oxygen-intolerant microbes (e.g., Muribaculaceae). Furthermore, we discussed potential impact of oxygen on the gut in various underlying critical illnesses involving inspiratory oxygen and peripheral VA-ECMO. Currently, the available findings in this area are somewhat controversial, and a consensus has not yet to be reached. It appears that targeting near-physiological oxygenation levels may offer a means to avoid hyperoxia-induced gut injury and hypoxia-induced mesenteric ischemia. However, the optimal oxygenation target may vary depending on special clinical conditions, including acute hypoxia in adults and neonates, as well as particular patients undergoing gastrointestinal surgery or VA-ECMO support. Last, we outlined the current challenges and the need for future studies in this area. Insights into this vital ongoing research can assist clinicians in optimizing oxygenation for critically ill patients.

Experience in applied veno-arterial extracorporeal membrane oxygenation to support catheter ablation of malignant ventricular tachycardia.

Background: An electrical storm due to malignant ventricular tachycardia (VT) is a life-threatening condition that requires catheter ablation (CA). Most VT arrhythmias evolve over time after acute myocardial infarction, coronary artery bypass grafting, or chronic heart failure. Clinically, only radiofrequency ablation can identify and block all arrhythmia origin points. The procedure necessitates continuous VT induction in patients, resulting in hemodynamic instability; therefore, extracorporeal membrane oxygenation (ECMO) support is required. Earlier studies have reported substantial mortality rates; however, our results are significantly more favorable. In this study, we combined the minimally invasive extracorporeal circulation (MiECC) approach with ECMO to preserve an appropriate ECMO flow rate, thus reducing intraoperative left heart afterload. We report 21 cases illustrating the usefulness of modified veno-arterial (VA)-ECMO in this scenario. Methods: Data of 21 patients supported by the modified VA-ECMO system (MiECC approach combined with the ECMO system) during VT CA in the Wuhan Asia Heart Hospital between June 2020 and July 2021 were reviewed retrospectively. Results: Successful ablation was achieved in 20 out of 21 patients (95%). The median time for ECMO implantation was 206 min. Only two patients experienced complications post-treatment. All patients made complete recovery and were discharged. All patients were alive at the 1-year-follow-up. Conclusions: Our modified VA-ECMO system helped restore systemic circulation in patients experiencing an electrical storm, thus achieving greater electrical stability during VT CA. Pre-insertion of VA-ECMO can achieve even better results.

ECMO combined with prone positioning strategies in COVID-19 respiratory distress syndrome.

The coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has already become a global pandemic as a public health emergency of international concern. Previous evidence from similar patient populations proved that carefully selected patients with severe ARDS who did not benefit from conventional treatment might be successfully supported with Veno-Venous extracorporeal membrane oxygenation (V-V ECMO). We now share the case reports of COVID-19 patients with ECMO combined prone position strategies.

In vivo quantification by SPECT of [123I] ADAM bound to serotonin transporters in the brains of rabbits.

BACKGROUND: A novel radioiodine ligand [(123)I] ADAM (2-((2-((dimethylamino)methyl)phenyl)thio)-5-iodophenylamine) has been suggested as a promising serotonin transporter (SERT) imaging agent for the central nervous system. In this study, the biodistribution of SERTs in the rabbit brain was investigated using [(123)I] ADAM and mapping images of the same animal produced by both single-photon emission computed tomography (SPECT) and microautoradiography. A semiquantification method was adopted to deduce the optimum time for SPECT imaging, whereas the input for a simple fully quantitative tracer kinetic model was provided from arterial blood sampling data. METHODS: SPECT imaging was performed on female rabbits postinjection of 185 MBq [(123)I] ADAM. The time-activity curve obtained from the SPECT images was used to quantify the SERTs, for which the binding potential was calculated from the kinetic modeling of [(123)I] ADAM. The kinetic data were analyzed by the nonlinear least squares method. The effects of the selective serotonin reuptake inhibitors fluoxetine and p-chloroamphetamine (PCA) on rabbits were also evaluated. After scanning, the same animal was sacrificed and the brain was removed for microautoradiography. Regions-of-interest were analyzed using both SPECT and microautoradiography images. The SPECT images were coregistered manually with the corresponding microautoradiography images for comparative study. RESULTS: During the time interval 90-100 min postinjection, the peak specific binding levels in different brain regions were compared and the brain stem was shown to have the highest activity. The target-to-background ratio was 1.89+/-0.02. Similar studies with fluoxetine and PCA showed a background level for SERT occupation. Microautoradiography demonstrated a higher level of anatomical details of the [(123)I] ADAM distribution than that obtained by SPECT imaging of the rabbit brain. CONCLUSION: SPECT imaging of the rabbit brain with [(123)I] ADAM showed high affinity, high specificity, and favorable kinetics. The time-activity curve showed that the accumulation of the [(123)I] ADAM in the brain stem reached a maximum between 90 and 100 min postinjection. The microautoradiography provides high-resolution images of the rabbit brain. Our results for the [(123)I] ADAM biodistribution in the rabbit brains demonstrate that this new radioligand is suitable as a selective SPECT imaging agent for SERTs.

Hypothermia attenuates circulatory shock and cerebral ischemia in experimental heatstroke.

We tested the hypothesis in a rat model that body cooling suppresses circulatory shock and cerebral ischemia in heatstroke. Animals under urethane anesthesia were exposed to water blanket temperature (Tblanket) of 42 degrees C until mean arterial pressure (MAP) and local cerebral blood flow (CBF) in the hippocampus began to decrease from their peak levels, which was arbitrarily defined as the onset of heatstroke. Control rats were exposed to 26 degrees C. Extracellular concentrations of glutamate, glycerol, lactate, and lactate/pyruvate in the hippocampus were assessed by microdialysis methods. Cooling was accomplished by decreasing Tblanket from 42 degrees C to 16 degrees C. The values of MAP and CBF after the onset of heat stroke in heatstroke rats received no cooling were all significantly lower than those in control rats. However, the neuronal damage score and extracellular levels of ischemia and damage markers in the hippocampus were greater. Cooling immediately after the onset of heatstroke reduced the heatstroke-induced circulatory shock, cerebral ischemia, neuronal damage, and surge of tissue ischemia and damage markers in the hippocampus, and resulted in prolongation of survival time. Delaying the onset of cooling reduced the therapeutic efficiency. The results suggest that body cooling attenuates circulatory shock and cerebral ischemia insults in heatstroke.

Hypothermia attenuates cerebral dopamine overloading and gliosis in rats with heatstroke.

The present study attempted to ascertain whether hypothermia attenuated the heat stroke-induced dopamine overload and gliosis in rat brain. Urethane-anesthetized rats were exposed to water blanket temperature (T(blanket)) of 42 degrees C until mean arterial pressure (MAP) began to decrease from their peak levels, which was arbitrarily defined as the onset of heat stroke. Extracellular concentrations of dopamine in brain were assessed by microdialysis methods. Hypothermia was accomplished by decreasing T(blanket) from 42 to 16 degrees C. The animals exposed to T(blanket) of 26 degrees C served as the normothermic controls. The values of MAP in heat stroke rats without hypothermia were all significantly lower than those in normothermic controls. However, the extracellular levels of dopamine and the number of glial fibrillary acidic protein-reactive cells in brain were greater. Hypothermia immediately after the onset of heat stroke reduced the heat stroke-induced circulatory shock as well as dopamine overload and gliosis in brain. The data demonstrate that hypothermia attenuates both dopamine overload and gliosis in rat brain associated with heatstroke.