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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Introduction: Although the effects on hemodynamics of gasping during cardiac arrest (CA) have received a lot of attention, less is known about the respiratory mechanics and physiology of respiration in gasping. This study aimed to investigate the respiratory mechanics and neural respiratory drive of gasping during CA in a porcine model. Method: Pigs weighing 34.9 ± 5.7 kg were anesthetized intravenously. ⋯ The partial pressure of oxygen showed a continuous decline after VF to reach statistical significance in the 10th minute (9.46 ± 0.96 kPa, P < 0.001), whereas the partial pressure of carbon dioxide tended to first rise and then fall. Conclusions: Gasping during CA was characterized by high VT , extremely low frequency, and prolonged expiratory time, which may improve hypercapnia. During gasping, increased work of breathing and insufficient neuromechanical efficacy of neural respiratory drive suggested the necessity of MV and appropriate management strategies for MV during resuscitation after CA.
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Background: Hemorrhagic shock-induced acute lung injury (ALI) is commonly associated with the posthemorrhagic shock mesenteric lymph (PHSML) return. Whether excessive autophagy is involved in PHSML-mediated ALI remains unclear. The relationship between estrogen treatment and PHSML or autophagy needs to verify. ⋯ E2 treatment significantly attenuated these adverse changes after hemorrhagic shock, which was reversed by PHSML or rapamycin administration. Importantly, PHSML incubation decreased the viability of pulmonary microvascular endothelial cells, while E2 coincubation or E2-treated lymph counteracted the adverse roles of PHSML. Conclusions: The role of estrogen reducing PHSML-mediated ALI is associated with the inhibition of autophagy.
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Pulmonary epithelial barrier injury contributes to acute lung injury, accelerating exudate formation, and resulting alveolar edema. Heme oxygenase-1 (HO-1) plays an important role in ameliorating the pathological symptoms of acute lung injury (ALI). Using an ALI mouse model induced by LPS inhalation, the present study explored the potential molecular regulatory effect of hemin (a potent HO-1 inducer) against ALI epithelial damage. ⋯ Furthermore, HO-1 elevation inhibited the activation of the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome and oxidative stress in alveolar epithelia, leading to the suppression of inflammatory responses and epithelial pyroptosis, as indicated by the decreased levels of NLRP3 and apoptosis-associated speck-like protein containing a CARD domain (ASC), repressed cleavage of caspase-1 and gasdermin D, and reduced expression levels of inflammatory cytokine IL-1β. In contrast, protoporphyrin IX zinc (II) (ZnPP, an HO-1 inhibitor) treatment had no protective effect on LPS inhalation-induced ALI in mice. In summary, HO-1 induction serves a critical role in maintaining airway epithelium homeostasis through the inhibition of NLRP3/ASC/caspase-1-mediated pyroptosis and inflammation in the occurrence of ALI.
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Randomized Controlled Trial Multicenter Study
Evaluation of Hydrocortisone, Vitamin C, and Thiamine for the Treatment of Septic Shock: A Randomized Controlled Trial (The HYVITS Trial).
Purpose: The aim of the study is to evaluate the effect of combined hydrocortisone, vitamin C, and thiamine (triple therapy) on the mortality of patients with septic shock. Methods : This multicenter, open-label, two-arm parallel-group, randomized controlled trial was conducted in four intensive care units in Qatar. Adult patients diagnosed with septic shock requiring norepinephrine at a rate of ≥0.1 μg/kg/min for ≥6 h were randomized to a triple therapy group or a control group. ⋯ Conclusion: Triple therapy did not improve in-hospital mortality at 60 days in critically ill patients with septic shock or reduce the vasopressor duration or SOFA score at 72 h. Trial Registration:ClinicalTrials.gov identifier: NCT03380507. Registered on December 21, 2017.
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Objective: Based on the functions of immunoregulation and signal transduction, septic peripheral blood sequencing and bioinformatics technology were used to screen potential core targets. Methods: Peripheral blood of 23 patients with sepsis and 10 normal volunteers underwent RNA-seq processing within 24 hours after admission to the hospital. Data quality control and differential gene screening were performed based on R language ( P < 0.01; log2FC ≥ 2). ⋯ Conclusions: CD160, KLRG1, S1PR5, and RGS16 were mainly located in human peripheral blood NK-T cells. Sepsis participants expressed lower levels of S1PR5, CD160, and KLRG1, while sepsis participants expressed higher levels of RGS16. This suggests that they may be potential research targets for sepsis.