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 objective was to examine the relationship of duration and magnitude of arterial hypotension to subsequent cellular immune suppression and cytokinemia in patients hospitalized with community-acquired pneumonia (CAP). We studied an observational cohort of 525 subjects hospitalized after presenting to the emergency department with radiographic and clinical signs of CAP. We compared the duration and magnitude of hypotension, using the cardiovascular Sequential Organ Failure Assessment (CV SOFA) subscore, to day 3 monocyte expression of human leukocyte antigen-DR (mHLA-DR), a previously validated marker of cellular immune suppression. ⋯ In patients admitted with CAP, arterial hypotension over the first 3 days is associated with markers of monocyte deactivation. The duration of exposure to hypotension may be more important than the magnitude, and monocyte deactivation correlates with IL-6 and IL-10 release. These results suggest that persistent hypotension might contribute to immunosuppression following septic shock.
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Early compliance with the sepsis resuscitation bundle has been suggested to reduce mortality. However, few data are available about the impact of late compliance with the bundle on outcomes. The aim of this study was to assess whether the completion of the resuscitation bundle within the first 6 h after admission to the intensive care unit (ICU), but beyond the specific time limit of the various bundle interventions, is related to an improvement in survival. ⋯ Importantly, similar results were found after excluding all patients with severe sepsis (rapid responders) and those with refractory shock (nonresponders). The task with highest improvement was the achievement of central venous oxygen saturation 70% or greater in 39% of patients. Compliance with the resuscitation bundle even beyond the recommended time is associated with improvement in survival in patients with severe sepsis/septic shock.
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This study tested the hypothesis that a novel mitochondria-targeted SS-31 peptide attenuates the burn injury-induced apoptosis and endoplasmic reticulum stress and improves insulin sensitivity in the skeletal muscle. Following 30% total body surface area burn or sham burn, mice were injected daily with SS-31 peptide (5 mg/kg body weight), and the rectus abdominis muscles collected on postburn days 1, 3, and 7. The tissues were subjected to various biochemical and immunohistochemical analyses. ⋯ Burn injury-induced increases in the levels of two endoplasmic reticulum stress markers, binding immunoglobulin protein and protein disulfide isomerase, were significantly decreased by the SS-31 peptide treatments on postburn day 7 and on day 3 for binding immunoglobulin protein as well (P < 0.05). The effects of SS-31 appear to be, in part, due to its ability to reduce oxidative stress in burned mice, evidenced by reduced expression of oxidized proteins that were clearly evident on postburn day 7. Our results demonstrate a possible therapeutic potential of SS-31 peptide to ameliorate the adverse effects of burn injury in skeletal muscle.
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Bronchial circulation plays a critical role in the pathophysiology of burn and smoke inhalation-induced acute lung injury. A 10-fold increase in bronchial blood flow is associated with excessive production of nitric oxide (NO) following smoke inhalation and cutaneous burn. Because an increased release of neuropeptides from the airway has been implicated in smoke inhalation injury, we hypothesized that direct delivery into the bronchial artery of low-dose 7-nitroindazole (7-NI), a specific neuronal NO synthase inhibitor, would attenuate smoke/burn-induced acute lung injury. ⋯ The increase in malondialdehyde and nitrate/nitrite in lung tissue was attenuated by treatment. Our data strongly suggest that local airway production of NO contributes to pulmonary dysfunction following smoke inhalation and burn injury. Most mechanisms that drive this pathophysiology reside in the airway.
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Hemorrhage is responsible for up to 40% of trauma mortality, and of these deaths, 33% to 56% occur during the prehospital period. In an effort to translate the cardioprotective effects of Adenocaine (adenosine, lidocaine) and Mg (ALM) from cardiac surgery to resuscitation science, we examined the early resuscitative effects of 7.5% NaCl with ALM in the rat model of 60% blood loss. Male Sprague-Dawley rats (250-350 g, n = 40) were anesthetized and randomly assigned to one of five groups: (a) untreated, (b) 7.5% NaCl, (c) 7.5% NaCl/6% dextran 70, (d) 7.5% NaCl/Mg, and (e) 7.5% NaCl/ALM. ⋯ At the end of phase 1, MAP of 7.5% NaCl/ALM-treated animals increased from 29 to 40 mmHg (P < 0.05). At the end of phase 2, MAP, PP, HR, and rate-pressure product in the ALM group were 75%, 193%, 96%, and 83% of their preshock values. Small-volume (∼1 mL/kg) i.v. bolus of 7.5% NaCl/ALM led to 100% survival following 60% blood loss with higher MAP than any group, an 89% to 96% reduction in the total number of arrhythmias, and a stable HR.