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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Comparative Study
Effect of body positions on hemodynamics and gas exchange in anesthetized pigs shortly after pneumonectomy.
Positional changes are thought to affect hemodynamics, respiratory mechanics, and gas exchange after pneumonectomy. The objective of this study was to compare hemodynamic and respiratory parameters and gas exchange in different positions before and after pneumonectomy. Twenty pigs were anesthetized and mechanically ventilated. ⋯ PaO2 was significantly higher in a lateral position, with the remaining lung uppermost. Our findings suggest that avoiding the supine positioning after pneumonectomy may facilitate improvements in hemodynamics and a decreased risk of hypoxemia. The optimal position for gas exchange after pneumonectomy is a lateral position, with the remaining lung in the uppermost position.
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Lung recruitment maneuvers (RMs), used to reopen atelectatic lung units and to improve oxygenation during mechanical ventilation, may result in hemodynamic impairment. We hypothesize that pulmonary arterial hypertension aggravates the consequences of RMs in the splanchnic circulation. Twelve anesthetized pigs underwent laparotomy and prolonged postoperative ventilation. ⋯ The corresponding recovery to at least 90% of baseline regional blood flow and organ perfusion lasted 1 to 5 min. Importantly, the decreases in regional blood flows and organ perfusion and the time to recovery of these flows did not differ from the controls. In conclusion, lipopolysaccharide-induced pulmonary arterial hypertension does not aggravate the RM-induced significant but short-lasting decreases in systemic, regional, and organ blood flows.
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There is substantial evidence that gut barrier failure is associated with distant organ injury and systemic inflammation. After major trauma or stress, the factors and mechanisms involved in gut injury are unknown. Our primary hypothesis is that loss of the intestinal mucus layer will result in injury of the normal gut that is exacerbated by the presence of luminal pancreatic proteases. ⋯ Because comparable levels of gut injury caused by systemic insults are associated with gut-induced lung injury, which is mediated by biologically active factors in mesenteric lymph, we next tested whether this local model of gut injury would produce active mesenteric lymph or lead to lung injury. It did not, suggesting that gut injury by itself may not be sufficient to induce distant organ dysfunction. Therefore, loss of the intestinal mucus layer, especially in the presence of intraluminal pancreatic proteases, is sufficient to lead to injury and barrier dysfunction of the otherwise normal intestine but not to produce gut-induced distant organ dysfunction.
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Sepsis and septic shock are frequently encountered in the intensive care unit. Despite the evolution of intensive care medicine during the last decades, septic shock is still associated with high mortality and complications of sepsis such as cholestasis, liver dysfunction, and massive intravascular volume deficit. Little is known about the whole pattern of changes at the transcriptional level during the development of acute sepsis. ⋯ Although after 21 h these animals are expected to die within the next 3 to 4 h from massive complications, functional induction of apoptosis could not be confirmed. Computer analysis identified three key regulator genes (IL8, CCL2, and CXCL2) among the first genes to be upregulated specifically in the sepsis group, and these can directly or indirectly control the bulk of the sepsis response. Induction of inflammatory mediators by sepsis was supported by the detection of corresponding cytokines (interleukin 6 and interleukin 8) in the blood.
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A dramatic decrease in circulating lymphocyte number is regularly described after septic shock. However, it is unknown how early this alteration develops after diagnosis of shock and if it remains stable over time. Twenty-one septic shock patients with no comorbidities were included within 2 h after the beginning of vasopressive treatment. ⋯ At the time of diagnosis of shock and admission in the intensive care unit, septic patients already present with severe lymphopenia involving every lymphocyte subsets including CD4 T-cell subpopulations. No significant variation could be detected within the first 48 h. This should be taken into account in the forthcoming clinical trials testing immunomodulating therapies in septic shock patients.