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 effect of analgesia on physiological systems has received little attention in trauma research. Our aim was to examine the effect of two different analgesics, buprenorphine and carprofen, on adenosine, lidocaine, and magnesium (ALM) resuscitation in a rat model of laparotomy and non-compressible hemorrhage. Male Sprague-Dawley rats were randomly assigned to Saline Carprieve, ALM Carprieve, Saline Buprenorphine, or ALM Buprenorphine (all n = 10). ⋯ No analgesic-related differences were found in total white cells, lymphocytes, platelet count, hyperthermia, weight loss, or pica. We conclude that reduced survival and MAP recovery appears to a buprenorphine effect on cardiovascular function. Until the underlying mechanisms can be elucidated, buprenorphine should be used with caution in small and possibly large models of trauma and shock.
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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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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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Altered postinjury platelet behavior is recognized in the pathophysiology of trauma-induced coagulopathy (TIC), but the mechanisms remain largely undefined. Studies suggest that soluble factors released by injury may inhibit signaling pathways and induce structural changes in circulating platelets. Given this, we sought to examine the impact of treating healthy platelets with plasma from injured patients. We hypothesized that healthy platelets treated ex-vivo with plasma from injured patients with shock would impair platelet aggregation, while treatment with plasma from injured patients with significant injury burden, but without shock, would enhance platelet aggregation. ⋯ Shock-mediated soluble factors impair platelet aggregation, and tissue injury-mediated soluble factors amplify platelet aggregation. Future characterization of these soluble factors will support development of novel treatments of TIC.