Masui. The Japanese journal of anesthesiology
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During several months of 2002, severe acute respiratory syndrome (SARS) caused by SARS-coronavirus (SARS-CoV) spread rapidly from China throughout the world causing more than 800 deaths due to the development of acute respiratory distress syndrome (ARDS). Interestingly, a novel homologue of angiotensin converting-enzyme (ACE), termed angiotensin converting enzyme 2 (ACE2) has been identified as a receptor for SARS-CoV. ACE and ACE2 share homology in their catalytic domain and provide different key functions in the renin-angiotensin system. ⋯ Importantly, our recent studies using ACE2 knockout mice have demonstrated that ACE2 protects murine lungs from ARDS. Furthermore, SARS-CoV infections and the Spike protein of the SARS-CoV reduce ACE2 expression. Notably, injection of SARS-CoV Spike into mice worsens acute lung failure in vivo that can be attenuated by blocking the renin-angiotensin pathway, suggesting the activation of pulmonary RAS influences the pathogenesis of ARDS and SARS.
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In this decade, the molecular mechanism of sepsis has been strikingly clarified. Especially, the identification of toll-like receptors as the pivotal molecules for the recognition of the stimulation of the inflammatory products of microorganisms has contributed to the elucidation of intracellular signaling pathways which result in severe systemic inflammatory response in sepsis. The production and release of a variety of pro-inflammatory mediators have been found to be associated with severe systemic inflammation and multiple organ dysfunction syndrome (MODS). ⋯ Despite of the advance in the basic research regarding molecular pathophysiology of sepsis, sepsis is still accompanied by high mortality in clinical settings. Almost all clinical trials targeting sepsis-associated mediators have failed, except the substitution therapy of activated protein C. However, further trials based on the basic findings, including the therapies targeting the multiple mediators, will contribute to the improvement of outcome of clinical sepsis. ple organ dysfunction syndrome (MODS), pro-inflammatory mediator, disseminated intravascular coagulopathy (DIC).
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A 14-year-old boy neurologically impaired was scheduled for tracheostomy under general anesthesia because of the prolonged tracheal intubation. He had twice received artificial respiration under tracheal intubation for aspiration pneumonia. During emergence from anesthesia, bucking occurred and suddenly the patient's lungs could not be ventilated. ⋯ SpO2 rapidly increased to normal range and heart rate recovered. The patient was suspected of having tracheomalacia as a result of flexible bronchoscopy performed through tracheostomy tube, revealing slight collapse of the trachea. Tracheomalacia can be a cause of sudden difficult ventilation in neurologically impaired children.
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We report a 38-year-old man with Kugelberg-Welander disease who underwent triple arthrodesis for talipes equinovarus under combined spinal-epidural anesthesia supplemented with continuous intravenous infusion of propofol. There was no ventilatory disturbance, muscle weakness, or neurologic untoward event during perioperative period.
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This special issue focuses on recent advances in understanding pathogenesis and altered physiology of sepsis on cellular and molecular basis. It is recognized that remarkable advances have been made in understanding the basic cellular and molecular mechanisms of multiple organ dysfunction associated with sepsis. ⋯ Although a lot of clinical trials have been conducted, a small number of treatment or management protocols have been proven to be effective in severe sepsis. Although critical questions remain unanswered, these new insights into sepsis-associated mechanisms are likely to lead to effective treatment approaches that ultimately improve clinical outcome.