Peroxides in human leucocytes in acute septic shock: a preliminary study of acute phase changes and mortality

Abstract

Peroxidation by peripheral blood leucocytes was measured in 15 patients in acute septic shock and 15 uninfected controls, using the probe dichloroflorescein. Mortality in septic subjects was 40%. In 14 of 15 patients from whom serial samples were analysed, periods of increased oxidative activity were detected. Increased peroxidation occurred early in the sequence of clinical changes, at the same time as increases in temperature, blood pressure and C-reactive protein. Peak peroxide production preceded increases in acute phase reactants and changes in leucocyte distribution. Mean peroxide production in leukocytes from patients who died was significantly higher (P < 0.001) than paired controls, and greater (P < 0.05) than peroxide production in patients who survived. The in vitro oxidative response to endotoxin was upregulated in infected patients. This supports the hypothesis that systemic mediators and leucocyte-derived reactive oxygen are involved in the vascular and organ damage associated with fatal septic shock.

Bacteraemia prediction in emergency medical admissions: role of C reactive protein

“…There may Table 2 Logistic regression models predicting bacteraemia in derivation set be indications for measuring CRP in acute medical patients, such as monitoring the progression of illness. [20][21][22] However, in the early detection of the most severe, bacteraemic forms of community acquired infection, the data presented here suggest that its role is limited. If the detection of severe infectious illness is the aim of using an acute inflammatory marker, and a full blood count is available, one needs to consider whether expending resources on CRP estimation is worthwhile.…”

Lymphocyte responses following open and minimally invasive thoracic surgery

“…The kinetics of reactive oxygen intermediate (ROI) production were analysed in lymphocytes from the same individual before and after stimulation. The rate of ROI generation was analysed using flow cytometric quantification of an oxidized probe in duplicate samples of patients and controls at 30‐sec intervals [ 36, 39–41]. Oxidative activity was determined 7 min before and 13 min after addition of n ‐6 essential fatty acid, using arachidonic acid (AA sodium salt; Sigma, Poole, UK) or gamma‐linolenic acid (GLA lithium salt; Scotia Pharmaceuticals, Stirling, UK) or saline control.…”

Identification of Glutathione S–Transferase Isozymes and γ–Glutamylcysteine Synthetase As Negative Acute–Phase Proteins in Rat Liver

“…It has been shown that the acute-phase response was also accompanied by metabolic changes and changes in the redox status. [23][24][25] Treatment of rats with either cytokines or poly dI-dC, an inducer of interferon, caused decreases in the protein and messenger RNA (mRNA) expression of cytochrome P450 enzymes, with resulting changes in hepatic metabolism, suggesting that at least some P450 enzymes behave as negative APPs [26][27][28][29][30][31][32][33][34][35][36][37][38] in humans as well. 39 Previously published data by Gallagher et al 40 show that chemically induced oxidative stress by intraperitoneal injection with the redox-cycling herbicide diquat caused a decrease in the expression of glutathione S-transferases (GSTs) and ␥-glutamylcysteine synthetase (GCS).…”