Avian influenza H10N3 is a type of avian influenza virus that can occasionally infect humans and cause severe pneumonia and acute respiratory distress syndrome (ARDS). On December 25, 2024, a 23-year-old obese female patient with H10N3 avian influenza complicated with severe ARDS was admitted to the Fourth People's Hospital of Nanning. The patient was transferred to our department due to "fever, cough, and shortness of breath for 13 days". Physical examination revealed moist rales in bilateral lungs. Chest imaging showed large areas of ground-glass opacity and consolidation in both lungs. Based on the patient's medical history, clinical manifestations, and laboratory findings, she was diagnosed with human infection of H10N3 avian influenza, severe pneumonia, and severe ARDS. Supported by mechanical ventilation and extracorporeal membrane oxygenation (ECMO), daily monitoring of airway peak pressure, plateau pressure (Pplat), driving pressure (ΔP), and lung compliance was performed to guide the adjustment of tidal volume (VT) and positive end-expiratory pressure (PEEP) during invasive mechanical ventilation. Medications including anti-avian influenza virus agents, antibacterial drugs, and antifungals were administered. Eventually, the patient's condition improved gradually, and she was successfully weaned from ECMO. No ventilator-induced lung injury (VILI) or multiple organ dysfunction syndrome (MODS) related to ARDS occurred during ECMO support. However, during the final stage of ventilator weaning after the restoration of spontaneous breathing, a right pneumothorax occurred. Closed thoracic drainage was performed, after which the ventilator was successfully discontinued. The patient was successfully transferred out of the intensive care unit (ICU), recovered fully, and was discharged from the hospital. In the invasive mechanical ventilation management of patients infected with H10N3 avian influenza complicated by ARDS, monitoring airway peak pressure, Pplat, ΔP, and assessing pulmonary compliance may facilitate more standardized management of such ARDS patients and help reduce VILI.
Humans ; Female ; Influenza, Human/complications* ; Respiratory Distress Syndrome/complications* ; Respiration, Artificial/methods* ; Obesity/complications* ; Young Adult ; Extracorporeal Membrane Oxygenation ; Influenza A virus

Objective: To explore lipid peroxidation injuries of pancreatic mitochondria and lysosome following severe acute pancreatitis (SAP) and the protective effects of gardenia jasminoides ellis (GJE) thereof. Methods: SAP models were induced by retrograde injection of 1.5% sodium deoxycholate. The rats were randomly divided into three groups: sham group, SAP group and GJE group. The changes were measured in superoxide dismutase (SOD), malondialdehyde (MDA), membrane fluidity of mitochondria and lysosome in pancreas and succinic dehydrogenase (SDH) in mitochondria, acid phosphatase (ACP) in lysosome.The effects of GJE were also observed. Results: Compared with Sham group, the activity of SOD and membrane fluidity of mitochondria and lysosome were decreased in pancreas, and the content of MDA were increased; the releasing rate of ACP was significantly higher in lysosome; SDH in mitochondria was lower in SAP group(P < 0.01). The above-mentioned indexes were obviously ameliorated in GJE group than those in SAP group(P < 0.01). The correlation analysis indicated that MDA was negatively correlated with SOD, positively correlated with membrane fluidity (P < 0.01). Conclusion: GJE can alleviate lipid peroxidation by getting rid of oxygen free radicals of pancreatic subcellular fraction in the course of SAP, and protect the structure and function of pancreatic subcellular fraction.

In the study we determined the content of malondialdehyde(MDA) , which is the metabolite of lipid peroxide(LPO) , in plasm and lung homogenate by thiobarbituric acid(TBA) colorimetry, and the content of phosphatidyl-choline(PC), which is the major functional composition of pulmonary surfactant (PS).and total phospholipid (TPL) by thin-layer chromatogra-phy and inorganic phosphorus quantitative analysis in rabbits with lung injury induced by oleic acid. The results showed that the MDA level wasincreased in plasm and lung homogenate; PC and TPL were decreased in lung homogenate. Administrating of 654-2 before and after (0. 5 h)lung injury could both inhibit the production LPO and prevent the decrease of PS. The findings suggest that the decrease of PS may be due to the increase of LPO and that G54-2 could modify the process.

The content of malondialdehyde (MDA) , a metabolite of lipid peroxide (LPO) , in plasma and tissue homongenate from rabbits with arrhythmias induced by adrenaline (Adr) was determined. The results showed that the MDA level was increased in plasma and tissue homogenate. Quinidine (Qui) 6 mg ? kg-1, Cimetidine (Cim) 37. 5 mg?kg-1, and 1/2 dose of both drugs administered intravenously couldsignificantly prevent ventricular arrhythmias induced by Adr and inhibit the production of MDA. The findings suggest that the effect of Qui and Cim on arrhythmias induced by Adr may associate with its inhibition on lipid peroxi-dation.