Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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The pathophysiology of traumatic hemorrhage is a phenomenon of vascular disruption and the symptom of bleeding represents one or more vascular injuries. In the Circulatory Trauma paradigm traumatic hemorrhage is viewed as injury to the circulatory system and suggests the underlying basis for endovascular hemorrhage control techniques. The question "Where is the patient bleeding?" is replaced by "Which blood vessels are disrupted?" and stopping bleeding becomes a matter of selective vessel access and vascular flow control. ⋯ This narrative review presents a brief overview of the current role of endovascular therapy in the management of circulatory trauma. The authors draw on their personal experience combined with the last decade of published experiences with the use of endovascular techniques in trauma and present general recommendations for their evolving use. The focus of the review is on the use of endovascular techniques as specific vascular treatments using the circulatory trauma paradigm.
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Acute lung injury (ALI) is caused by direct pulmonary insults and indirect systemic inflammatory responses that result from conditions such as sepsis and trauma. Alveolar macrophages are the main and critical leukocytes in the airspace, and through the synthesis and release of various inflammatory mediators critically influence the development of ALI following infection and non-infectious stimuli. ⋯ In this study, we demonstrate that memantine, a N-methyl-D-aspartic acid receptor (NMDAR) antagonist, through suppressing Ca2+ influx and subsequent ASC oligomerization inhibits macrophage Nlrp3 inflammasome activation and pyroptosis, therefore, alleviates ALI in septic mice. This finding explores a novel application of memantine, an FDA already approved medication, in the treatment of ALI, which is currently lacking effective therapy.
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Septic cardiac dysfunction remains a clinical problem due to its high morbidity and mortality. Uncontrolled cell death and excessive inflammatory response are closely related to sepsis-induced cardiac dysfunction. Irisin has been found to play cardioprotective roles in sepsis. ⋯ However, irisin can inhibit the expression of TLR4 and its downstream signaling molecules and also lower the level of apoptosis and pyroptosis. Besides, similar results were also found in vitro model of LPS-induced H9c2 cardiomyocyte injury. In general, irisin suppressed inflammation, apoptosis, and pyroptosis by blocking the TLR4 and NLRP3 inflammasome signalings to mitigate myocardial dysfunction in sepsis.