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
-
In septic shock (SS), dysfunction of many organ systems develops during the course of the illness, although the mechanisms are not clear. In earlier studies, we reported that lysozyme-c (Lzm-S), a protein that is released from leukocytes and macrophages, was a mediator of the myocardial depression and vasodilation that develop in a canine model of Pseudomonas aeruginosa SS. Whereas both of these effects of Lzm-S are dependent on its ability to intrinsically generate hydrogen peroxide, we subsequently showed that Lzm-S can also deposit within the vascular smooth muscle layer of the systemic arteries in this model. ⋯ In the in vivo model, Lzm-S accumulated in the kidney and the superior mesenteric artery. In a canine renal epithelial preparation, we further showed that Lzm-S can be taken up by the renal tubules to activate inflammatory pathways. We conclude that Lzm-S can deposit in the systemic vasculature and kidneys in SS, where this deposition could lead to acute organ dysfunction.
-
Sepsis and sepsis-induced organ dysfunction remain lethal and common conditions among intensive care patients. Accumulating evidence suggests that the matricellular Cyr61/CCN1 (cysteine-rich, angiogenic-inducer, 61) protein is involved in the regulation of inflammatory responses and possesses organ-protective capabilities in diseases of an inflammatory etiology. However, its regulation in sepsis remains largely unexplored. ⋯ Both agonists induced an instant CCN1 release, and the effect of SFLLRN was blocked by the specific antagonist RWJ56110. The current study demonstrates that experimental sepsis is associated with a robust increase in circulating CCN1 protein levels and a paradoxical downregulation of CCN1 mRNA expression in vital organs. It provides evidence that CCN1 is released from activated platelets, suggesting that platelets constitute a novel source for CCN1 release to the circulation during sepsis.
-
Clinical Trial Observational Study
Plasma Colloid Osmotic Pressure is an Early Indicator of Injury and Hemorrhagic Shock.
Hemorrhagic shock is the leading cause of traumatic deaths; many could be potentially prevented with appropriate resuscitation. However, to initiate resuscitation, one must identify patients with hemorrhagic shock early. In this article, we determined the associations between plasma colloid osmotic pressure (COP) and clinical outcomes in severely injured trauma patients. ⋯ Reduced plasma COP and serum protein in trauma patients are indicative of injury severity. In the absence of significant alterations in vital signs, plasma COP levels were associated with increased requirements for blood products and increased syndecan 1 shedding. We believe that plasma COP provides new insight in guiding resuscitation.
-
Comparative Study Clinical Trial
Racial Differences in Vasopressor Requirements For Septic Shock.
The objective of this study was to compare vasopressor requirements between African American (AA) patients and white patients in septic shock. ⋯ African American patients with septic shock were treated with higher doses of NE and required longer duration of NE administration compared with white patients.
-
Codonopsis pilosula polysaccharide (CPPS) isolated from one of the Chinese herbs is known to have a variety of immunomodulatory activities. However, it is not clear whether CPPS can exert an effect on the immune functions of regulatory T cells (Tregs). This study was carried out to investigate the effect of CPPS on the immune function of peripheral blood Tregs in sepsis induced by cecal ligation and puncture (CLP). ⋯ Codonopsis pilosula polysaccharide might suppress excessive Tregs, at least in part, via TLR4 signaling on Tregs and trigger a shift of TH2 to TH1 with activation of CD4 T cells in sepsis induced by CLP.