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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Traumatic brain injury (TBI) can induce acute lung injury (ALI). The exact pathomechanism of TBI-induced ALI is poorly understood, limiting treatment options. Remote ischemic conditioning (RIC) can mitigate detrimental outcomes following transplants, cardiac arrests, and neurological injuries. ⋯ However, there was no RIC-associated change in plasma irisin or S1P. At 7 DPI, ALI in TBI mice was largely resolved, with evidence for residual lung pathology. Thus, RIC may be a viable intervention for TBI-induced ALI to preserve lung function and facilitate clinical management.
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As an integral component of cardiac tissue, macrophages are critical for cardiac development, adult heart homeostasis, as well as cardiac healing. One fundamental function of macrophages involves the clearance of dying cells or debris, a process termed efferocytosis. Current literature primarily pays attention to the impact of efferocytosis on apoptotic cells. ⋯ Therefore, understanding macrophage efferocytosis would provide valuable insights on cardiac health, and may offer new therapeutic strategies for the treatment of patients with heart failure. In this review, we first summarize the molecular signals that are associated with macrophage efferocytosis of apoptotic and necrotic cells, and then discuss how the linkage of efferocytosis to the resolution of inflammation affects cardiac function and recovery under normal and diseased conditions. Lastly, we highlight new discoveries related to the effects of macrophage efferocytosis on cardiac injury and repair.
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Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are caused by an exaggerated inflammatory response arising from a wide variety of pulmonary and systemic insults. Lung tissue is composed of a variety of cell populations, including parenchymal and immune cells. ⋯ To date, the question of how different types of pulmonary cells communicate with each other and subsequently regulate or modulate inflammatory cascades remains to be fully addressed. In this review, we provide an overview of current advancements in understanding the role of cell-cell interaction in the development of ALI and depict molecular mechanisms by which cell-cell interactions regulate lung inflammation, focusing on inter-cellular activities and signaling pathways that point to possible therapeutic opportunities for ALI/ARDS.
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Neutrophils play a critical role in the eradication of pathogenic organisms, particularly bacteria. However, in the septic patient the prolonged activation and accumulation of neutrophils may augment tissue and organ injury. ⋯ Delayed neutrophil apoptosis may contribute to organ injury, or allow better clearance of pathogens. Neutrophils provide a friendly immune response to clear infections, but excessive activation and recruitment has the potential to turn them into potent foes.
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Alternation in traditional vital signs can only be observed during advanced stages of hypovolemia and shortly before the hemodynamic collapse. However, even minimal blood loss induces a decrease in the cardiac preload which translates to a decrease in stroke volume, but these indices are not readily monitored. We aimed to determine whether minor hemodynamic alternations induced by controlled and standardized hypovolemia can be detected by a whole-body bio-impedance technology. ⋯ Continuous noninvasive monitoring of SV may be superior to conventional indices (e.g., heart rate, blood pressure, or shock index) for early identification of acute blood loss. As an operator-independent and point-of-care technology, the SV whole body bio-impedance measurement may assist in accurate monitoring of potentially bleeding patients and early identification of hemorrhage.