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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To monitor the ischemic and/or reperfusion injury after porta hepatis occlusion (Pringle maneuver) in livers subjected to hypotension, serum alanine amino transferase (ALT), liver malondialdehyde (MDA), and liver glutathione (GSH) levels were measured. MDA is a by-product of oxidant-induced lipid peroxidation, and GSH is an endogenous antioxidant. The effects of lactated Ringer's (LR) and hypertonic saline (7.5%)/Dextran (6%; HSD) resuscitation on liver injury, if any, was investigated. ⋯ Liver tissue MDA was 353 +/- 22 nmol/g/tissue in the HI group and LR decreased it to 261 +/- 17 nmol/g/tissue, whereas HSD decreased it to 273 +/- 20 nmol/g/tissue. The decrease in ALT and the increase in liver GSH were more pronounced with HSD resuscitation (P < 0.05). HSD seems to be more effective than LR in decreasing the liver tissue damage produced by total hepatic inflow occlusion under hypovolemic conditions.
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Comparative Study
Serum S 100 B: a marker of brain damage in traumatic brain injury with and without multiple trauma.
This prospective clinical study was conducted to determine whether S 100 B is a reliable serum marker for traumatic brain injury (TBI) with and without multiple trauma. Fifty-five trauma patients (Injury Severity Score [ISS] > or = 24 and Glasgow Coma Score [GCS] < or = 8) were classified by radiography, computer tomography, ultrasound, and neurology as TBI without multiple trauma (n = 23), TBI with multiple trauma (n = 23), or multiple trauma without TBI (n = 9). S 100 B was measured initially after trauma and daily for a maximum of 21 days. ⋯ According to receiver operating characteristic curve analysis and calculation of the area under the curve (AUC), S 100 B is equally accurate for mortality prediction at 24, 48, and 72 h after trauma and is most accurate >84 h after trauma. Sensitivity/specificity for mortality prediction are more accurate in TBI without multiple trauma (AUC 0.802-0.971) than in TBI with multiple trauma (AUC 0.693-0.783). Thus, though S 100 B may be a reliable marker of brain damage in TBI without multiple trauma 24 h after trauma and thereafter, it appears to be less reliable in TBI with multiple trauma.
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Comparative Study
Endothelium-dependent vasodilation in the skin microcirculation of patients with septic shock.
The evidence for endothelial dysfunction in sepsis is mostly restricted to animal models. We investigated endothelial function in the skin microcirculation of eight patients hospitalized for septic shock in an intensive care unit (ICU). All patients required adrenergic support. ⋯ The ratio of responses to Ach and SNP did not significantly differ between groups (septic: 1.22 +/- 0.40; ICU control 1.18 +/- 0.46, healthy, nonsmoking 1.12 +/- 0.24, P = 0.86). Thus, sepsis was not associated with a selective depression of the endothelium-dependent response. These results suggest that the capacity of the endothelium to produce signals for vasorelaxation remains intact in the skin microcirculation of patients with septic shock.
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It has been demonstrated that lipopolysaccharide (LPS)-induced cytokine response in patients with sepsis differ from the normal host, yet this has not been controlled for the presence of underlying disease. We studied the ability of LPS and killed gram-negative bacteria (GNB) to induce tumor necrosis factor (TNF)-alpha and interleukin (IL) 10, and of phytohemagglutinin (PHA) to induce interferon (IFN)-gamma, in whole blood from patients with sepsis (SP, n = 20), patients with matched underlying disease and without sepsis (control patients, n = 20), and healthy volunteers (HV, n = 20). LPS-induced TNF-alpha production was lower in SP (median = 638 pg/mL) compared with control patients (4060 pg/mL; P= 0.003), and control patients production was lower compared with HV (5329 pg/mL; P < 0.001). ⋯ IL-10 production was not different among the three groups. Down-regulation of TNF-alpha production in patients with sepsis, although not restricted to them, was more pronounced with LPS than with GNB. Although the presence of underlying disease may be involved in the regulatory mechanisms of host response, the use of controls with matched underlying diseases provides strong evidence for the septic condition in the down-regulation of inflammatory response in patients with sepsis.
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The systemic inflammatory response syndrome results from an uncontrolled, overexpression of the normal host inflammatory response, leading to destruction of host tissue and subsequent organ failure. Oxidant stress has been implicated in this process both as a mechanism for direct cellular injury, as well as activation of intracellular signaling cascades within inflammatory cells resulting in progression of the inflammatory response. Vitamin E is an inexpensive, nontoxic, chain-breaking antioxidant that has therapeutic potential in regulating this process. This review seeks to evaluate the current literature regarding the use of Vitamin E in controlling the excessive inflammation seen in systemic inflammatory response syndrome and argues for further study of its therapeutic potential for these critically ill patients.