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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Sepsis-associated encephalopathy (SAE) represents a severe complication of sepsis, substantially elevating both mortality and healthcare costs for patients. Gastrodin (GAS), a principal bioactive constituent of Gastrodia elata Blume, is neuroprotective in various neurological disorders, including ischemic stroke, epilepsy, Alzheimer's disease, and neuropathic pain. In this study, we sought to investigate whether GAS could serve as a protective agent against SAE. ⋯ Our study elucidated that GAS offers protection against SAE by suppressing ferroptosis through the activation of the COX-2/PGE2/GPX4 axis. This research validates the therapeutic potential of GAS and provides novel insights into potential therapeutic strategies for the management of SAE.
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Loss of muscle mass and strength in patients who have experienced severe burns is dramatic and associated with subsequent functional impairment. Past work has shown that exercise and oxandrolone, an anabolic steroid, individually improve muscle function and muscle mass in severely burned patients. This study aims to evaluate the effect of oxandrolone treatment combined with resistance exercise on muscle atrophy and investigate the protein synthesis and mitochondrial biogenesis pathways in a hindlimb suspension model. ⋯ Oxandrolone and resistance exercise have independent positive effects on muscle function recovery in this clinically relevant rodent model of severe burn. Both treatments combined increased signaling pathways by increasing protein synthesis.
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While acute myocardial infarction (AMI) is widely recognized as the primary cause of Cardiogenic Shock (CS), Non-AMI related CS has been excluded from the majority of CS studies. Information on its prognostic factors remains largely understudied, and it is necessary to focus on these patients to identify the specific risk factors. In this study, we aimed to build and validate a predictive nomogram and risk classification system. ⋯ For non-AMI associated CS, a predictive nomogram and risk classification system were developed and validated, and the nomogram demonstrated good performance in prognostic prediction and risk stratification.
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Intestinal ischemia-reperfusion injury is associated with both macrocirculatory and microcirculatory failure. Association of a vasoconstrictor in combination with a vasodilator such as ilomedin may improve macrocirculation parameters, microcirculation perfusion and reduce endothelial dysfunction. The primary objective was to demonstrate a difference in mean arterial pressure (MAP) after intestinal reperfusion with the concomitant administration of norepinephrine and ilomedin during ischemia compared with traditional hemodynamic treatment strategies (fluid resuscitation and vasopressors only). Secondary objectives were to demonstrate an improvement in peripheral and intestinal microcirculatory perfusion and endothelial dysfunction after intestinal reperfusion using this association. ⋯ Early administration of norepinephrine and ilomedin during ischemia improved short-term post-reperfusion sublingual and intestinal microcirculation without worsening macrocirculatory parameters in an intestinal ischemia-reperfusion injury model. However, use of this strategy seemed to worsen both liver and kidney function.
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Background: Sepsis continues to pose a significant threat to human life and represents a substantial financial burden. In addition to replicative stress resulting from telomeric loss, recent studies have identified multiple factors contributing to cell cycle arrest. Furthermore, our understanding of pathways associated with cellular senescence, such as CD47-mediated suppression of efferocytosis, has expanded. ⋯ Later, at 7 d after CLP, pulmonary expression of CD47 and QPCTL-1 was decreased, whereas SHP-1 was significantly enhanced. Conclusion: Our findings suggest an activation of senescent-associated pathways during experimental sepsis. However, expanding the experiments to other organ systems and in vivo long-term models are necessary to further evaluate the sustained mechanisms and immunopathophysiological consequences of cellular senescence triggered by septic organ injury.