Lipid peroxidation in rat lung induced by neuroleptanalgesia and its components.

The aim of the present work was to determine the likelihood of lipid peroxidation in the lungs of rats subjected to neuroleptanalgesia and its components. In particular, the effect of fentanyl, droperidol, a nitrous oxide/oxygen mixture when used separately or in combination, on the lung level of lipid peroxidation was investigated. The in vitro antioxidant properties of fentanyl and droperidol were also tested. Lipid peroxidation was evidenced by the endogenously generated conjugated dienes and fluorescent products of lipid peroxidation and the decrease in lung vitamin E content. It was found that fentanyl and droperidol, used separately or in combination, did not induce lipid peroxidation in the rat lung, while the exposure of rats for 120 min to a nitrous oxide/oxygen mixture (2:1 v/v) led to well-expressed peroxidation. The (N2O + O2)-pro-oxidant action was significantly inhibited in rats previously injected with fentanyl and/or droperidol. The results show that the application of fentanyl, droperidol and (N2O + O2), as in neuroleptanalgesia, ensures minimal lipid peroxidation in the lung. In addition, we found that fentanyl and droperidol were able to inhibit the Fe(2+)-catalysed lipid peroxidation in lung homogenate. We speculate that the inhibitory effect of fentanyl and/or droperidol on the (N2O + O2)-induced lipid peroxidation in the rat lung may be caused directly by their antioxidant properties. However, another explanation seems to be possible. The free radicals that are produced during the metabolism of fentanyl and droperidol may react with the radicals generated during the one-electron reduction of nitrous oxide. Such reactions will obviously reduce the free radical concentration in the organism and, hence, the likelihood of initiating lipid peroxidation.

Nitrous oxide with fentanyl and droperidol minimizes lipid peroxidation in the liver.

We have studied the level of lipid peroxidation in the liver of rats exposed to nitrous oxide plus oxygen or injected with droperidol of fentanyl. The effect of nitrous oxide used in combination with droperidol and fentanyl was also investigated. All the tested anaesthetics caused lipid peroxidation in the rat liver. It seems likely, however, that the mechanism by which droperidol and fentanyl initiate lipid peroxidation differs from that which nitrous oxide uses. Free radical products and/or activated oxygen species are produced during fentanyl and droperidol metabolism in the liver. However, nitrous oxide is not metabolized in the liver and probably undergoes one electron reduction outside the liver thus producing free radical products and/or activated oxygen species which are able to diffuse and initiate lipid peroxidation in the liver. It was also found that the level of lipid peroxidation in the liver of rats injected with droperidol and fentanyl and then exposed to nitrous oxide was low and close to that of the control animals. We suggest that, when used in combination, the products generated outside the liver as a result of nitrous oxide metabolism are transported to the liver and take part in reactions with the products of the metabolism of droperidol and fentanyl, thus decreasing the concentration of the species able to initiate lipid peroxidation.