SUMMARY After trauma, inflammatory, immunological and hormonal changes are well documented. Surgical intervention is a form of programmed trauma. Through the study of surgical patients, changes in early endogenous mediators of inflammation, immune response and tissue repair can be investigated. Here we analysed changes in serum levels of IL‐1 inhibitors, IL‐1β, IL‐6, tumour necrosis factor‐alpha (TNF‐α) and cortisol in patients undergoing elective surgery. C‐reactive protein (CRP) was measured as a marker of the acute‐phase response. Rises in serum levels of IL‐1 inhibitors. IL‐6 and cortisol were detected as early as 1 h after the intervention. Peak levels were reached between 2 and 5 h. Serum levels of IL‐6 and cortisol remained elevated for several days implying a persistent production. Serum levels of IL‐1 and TNF did not change after the intervention. CRP levels peaked on day 2. The communication system sustained by endogenous mediators is activated after surgery as shown by selective changes in IL‐1 inhibitors, IL‐6 and cortisol. These mediators have different kinetics in serum and IL‐6 is not the only early mediator detected. Some IL‐1 inhibitors might be involved in the immunological depression observed after major surgery, in the regulation of the inflammatory response or in tissue repair. IL‐6 and cortisol seem to act synergistically to activate the acute‐phase response. A systemic role for IL‐l and TNF is not evident, even if the possibility that these lymphokines may act locally is not ruled out.

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Epidemiological investigations have revealed that alcoholic cirrhosis is associated with a high frequency of pigment gallstones, but only scanty information is available on the effects of ethanol on biliary secretion of bilirubin. We have injected intravenously 1.0 and 1.5 g/kg body wt of ethanol into six cholecystectomized rabbits and a common bile duct fistula. Experiments were performed ten days after surgery and a stream-splitting apparatus was interposed in the circuit in order to withdraw continuously biliary samples without interruption of enterohepatic bile circulation. Analysis of hourly data showed that both ethanol doses significantly increase the biliary concentration of total bilirubin, without affecting bile flow and lipid composition. Alcohol also promoted the efflux of unconjugated bilirubin into bile. The maximum effect occurred within the first 5 hr following alcohol administration. Thereafter the bile returned to normal. Since excessive concentrations of biliary unconjugated bilirubin favor pigment gallstone development, it can be speculated that alcohol acts as a risk factor for pigment lithiasis by enhancing the biliary levels of this form of pigment.

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