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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Clinical Trial
Association of Clinical Hypoperfusion Variables With Lactate Clearance and Hospital Mortality.
Lactate has shown utility in assessing the prognosis of patients admitted to the hospital with confirmed or suspected shock. Some findings of the physical examination may replace it as screening tool. We have determined the correlation and association between clinical perfusion parameters and lactate at the time of admission; the correlation between the change in clinical parameters and lactate clearance after 6 and 24 h of resuscitation; and the association between clinical parameters, lactate, and mortality. ⋯ Among patients with hypoperfusion risk or shock, no correlation was found between clinical variables and lactate. Of the set of parameters collected, lactate at admission was the only independent marker of mortality.
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Comparative Study
Effects of Dextran-70 and Albumin on Coagulation in Experimental Hemorrhage in the Guinea Pig.
Dextran-70 is a more potent plasma volume expander than albumin but use has been hampered because of its antithrombotic properties. However, also albumin has antithrombotic properties and little is known about relative effects of these two colloids on coagulation in vivo when controlling for differences in efficacy as plasma volume expanders. ⋯ In equipotent doses with regard to plasma volume expansion, dextran-70 transiently prolongs clot amplification time more than albumin whereas dextran-70 reduces plasma vWF concentrations less than albumin.
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Stearoyl lysophosphatidylcholine (LPC) exerts protective effect during endotoxemia and in experimental sepsis, but the underlying mechanism is unclear. Here, we demonstrated that stearoyl LPC could block caspase-11-mediated macrophage pyroptosis. In vitro, stearoyl LPC significantly decreased caspase-11 activation and pyroptosis induced by lipopolysaccharide (LPS) plus cholera toxin subunit B independent of the receptor G2A. ⋯ Moreover, stearoyl LPC treatment conferred significant protection against lethal endotoxemia and significantly reduced the release of IL-1α and IL-1β. These findings identify stearoyl LPC as an inhibitor of LPS-mediated caspase-11 activation. This mechanism could explain the protective action of stearoyl LPC in experimental sepsis and endotoxemia.
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Decompensation, a critical phase in the response to hemorrhage, is characterized by profound sympathoinhibition and the overriding of baroreflex mediated compensation. As sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) maintain vasomotor tone and are essential for sympathetic baroreceptor reflex function, the RVLM is the likely mediator. However, how decompensation occurs is a mystery. ⋯ However, SST2 receptor antagonists bilaterally injected in the RVLM or the A1 region did not affect the decompensation response to hemorrhage. Thus somatostatin in the RVLM does not mediate decompensation. The physiological role associated with somatostatin-induced sympathoinhibition in the RVLM together with the central mechanisms responsible for decompensation remain elusive.
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Observational studies show a peak incidence in cardiovascular events during and early after clinical conditions associated with substantial systemic inflammation, such as pneumonia. The acuteness of this increased risk suggests rapid plaque destabilization and associated intraplaque inflammation. We evaluated whether lipopolysaccharides (LPS)-evoked acute systemic inflammation would induce such detrimental vascular changes in murine aortas with manifest atherosclerotic lesions. ⋯ Intraperitoneal LPS injection in ApoE3*Leiden mice triggers a profound systemic inflammatory response, but does not increase atherosclerotic plaque area or inflammatory cell density. This model of LPS-induced inflammation in atherosclerosis-prone mice argues against intraplaque alterations as an explanation for acute inflammation-induced cardiovascular event risk.