We could not demonstrate overproduction of anti-inflammatory IL-10 in MOF patients. On the contrary, the high IL-6/IL-10 ratio indicates that IL-10 deficiency may contribute to the development of MOF in severe sepsis.

Purpose:We investigated whether propofol at a sedative dose can prevent intestinal mucosa ischemia/reperfusion (I/R) injury, and if propofol can attenuate oxidative stress and increases in nitric oxide (NO) and endothelin-1 (ET-1) release that may occur during intestinal I/R injury. Methods:Rats were randomly allocated into one of five groups (n = 10 each): (i) sham control; (ii) injury (one hour superior mesenteric artery occlusion followed by three hours reperfusion); (iii) propofol pre-treatment, with propofol given 30 min before inducing intestinal ischemia; (iv) simultaneous propofol treatment, with propofol given 30 min before intestinal reperfusion was started; (v) propofol post-treatment, with propofol given 30 min after intestinal reperfusion was initiated. In the treatment groups, propofol 50 mg·kg -1 was administrated intraperitoneally. Animals in the control and untreated injury groups received equal volumes of intralipid (the vehicle solution of propofol) intraperitoneally. Intestinal mucosa histology was analyzed by Chiu's scoring assessment. Levels of lactic acid (LD), NO, ET-1, lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD) activity in intestinal mucosa were determined. Results:Histological results showed severe damage in the intestinal mucosa of the injury group accompanied by increases in MDA, NO and ET-1 and a decrease in SOD activity. Propofol treatments, especially pre-treatment, significantly reduced Chiu's scores and levels of MDA, NO, ET-1 and LD, while restoring SOD activity. Conclusion:These findings indicate that propofol attenuates intestinal I/R-induced mucosal injury in an animal model. The response may be attributable to propofol's antioxidant properties, and the effects of inhibiting over-production of NO and in decreasing ET-1 levels. CAN J ANESTH 2007 / 54: 5 / pp 366-374 Objectif : Nous avons cherché à savoir si le propofol, en dose sédative, pouvait empêcher les lésions d'ischémie/reperfusion (I/R) de la muqueuse intestinale, et s'il pouvait atténuer le stress oxydatif et les augmentations dans la libération d'oxyde nitrique (NO) et d'endothéline-1 (ET-1) pouvant survenir lors de lésions I/R intestinales. Méthode : Des rats ont été randomisés en cinq groupes (n = 10 chacun) : (i) faux témoin (sham control) ; (ii) lésion (occlusion de

The ICU stay was longer and multiple organ failure more severe in patients with impaired adrenocortical function. There was a clear dissociation between ACTH and cortisol levels in AAR patients. This finding suggests that the integrity of the hypothalamic-pituitary-adrenal axis may be impaired in severe sepsis.

As an original finding, we report here that resistin levels correlate with oxidative stress and myocardial injury in patients undergoing cardiac surgery. In addition, leptin levels were increased on the first postoperative day, but only minor declines were found in adiponectin and adipsin levels. Resistin has been implicated in unfavourable metabolic, cardiovascular and inflammatory responses: it may thus serve as a useful biomarker or a drug target in conditions complicated by ischaemia-reperfusion injury.

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