Summary

The ‘wet vs. dry’ philosophy in patients undergoing abdominal surgery is a subject of substantial debate. It has been suggested that restricting fluid input would significantly reduce complications and improve outcome following abdominal surgery. Keeping the patients dry may be a two-edged sword because the resulting hypovolaemia may result in compromised organ perfusion and poor tissue oxygenation. A review of the literature from 1990 to 2004 revealed that only very few studies on this subject have been published. Unfortunately, most of the ‘dry’-supporting studies used fixed amounts of volume instead of a fluid concept adapted to the patients' need (‘goal-directed’) and there is no generally accepted definition of ‘restricted’, ‘dry’ or ‘overload’. Not only the amount but also the kind of administered fluid appears to be important. Current evidence indicates that using crystalloids exclusively may cause overloading of the interstitial compartment with considerable negative sequelae, whereas using colloids may improve microperfusion and tissue oxygenation. This review shows that the meagre literature on a restricted volume replacement strategy in abdominal surgery patients cannot clearly support the ‘dry’ approach. Further well-performed studies are necessary to elucidate the ideal amount and type of fluid replacement and determine how to guide fluid therapy.

Background and objective Respiratory burst is an essential component of the neutrophil's biocidal function. In vitro, sodium thiopental, isoflurane and lidocaine each inhibit neutrophil respiratory burst. The objectives of this study were (a) to determine the effect of a standard clinical induction/tracheal intubation sequence on neutrophil respiratory burst and (b) to determine the effect of intravenous lidocaine administration during induction of anaesthesia on neutrophil respiratory burst.

Methods Twenty ASA I and II patients, aged 18–60 years, undergoing elective surgery were studied. After induction of anaesthesia [fentanyl (2 μg kg−1), thiopental (4–6 mg kg−1), isoflurane (end-tidal concentration 0.5–1.5%) in nitrous oxide (66%) and oxygen], patients randomly received either lidocaine 1.5 mg kg−1 (group L) or 0.9% saline (group S) prior to tracheal intubation. Neutrophil respiratory burst was measured immediately prior to induction of anaesthesia, immediately before and 1 and 5 min after lidocaine/saline.

Results Neutrophil respiratory burst decreased significantly after induction of anaesthesia in both groups [87.4 ± 8.2% (group L) and 88.5 ± 13.4% (group S) of preinduction level (P < 0.01 both groups)]. After intravenous lidocaine (but not saline) administration, neutrophil respiratory burst returned towards preinduction levels, both before (97.1 ± 23.6%) and after (94.4 ± 16.6%) tracheal intubation.

Conclusion Induction of anaesthesia and tracheal intubation using thiopentone and isoflurane, inhibit neutrophil respiratory burst. This effect may be diminished by the administration of lidocaine.

Following hints from X-ray data (Ostermeier C et al., 1997, Proc Natl Acad Sci USA 94:10547–10553; Yoshikawa S et al., 1998, Science 280:1723–1729), chemical evidence is presented from four distantly related cytochrome-c oxidases for the existence of a copperB-coordinated His240–Tyr244) cross-link at the O2-activating Heme Fea3–CuB center in the catalytic subunit I of the enzyme. The early evolutionary invention of this unusual structure may have prevented demaging [bull ]OH-radical release at e−-transfer to dioxygen and thus have enabled O2 respiration.