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No abstract

Tourniquet ischemia will influence the biochemical milieu of tissue cells and affect the metabolism of purines in skeletal muscle distal to the occlusion. At reperfusion, generation of oxygen radicals by the hypoxanthine-xanthine oxidase system may ensue, influencing white blood cell and thrombocyte aggregation, causing damage to the endothelial cell barrier and inducing non-reflow type phenomena. Amide-type local anaesthetics are known to affect local vasotone, leukocyte adherence and platelet function but the influence of lidocaine on purine metabolite washout and platelet aggregation following tourniquet ischemia for lower limb surgery is not known in detail. Therefore, the effects of regional intravenous lidocaine during tourniquet ischemia for knee surgery on purine catabolite washout and platelet function following reflow were assessed. Eight patients served as control (C-group) and 8 (L-group) received 100 ml of lidocaine (2.5 mg/ml) in the emptied venous bed of the leg to be operated. All patients had spinal anaesthesia (0.5% bupivacaine). Effluent venous blood from the leg and radial arterial blood was collected and analysed for xanthine (X), hypoxanthine (HX), base excess (BE), pH and potassium before and after reperfusion. Platelet ADP-induced aggregation (ADP-agg.) and secretion of beta-thromboglobulin (beta-TG) were measured in the effluent blood as well as systemically. After tourniquet release (TR), X and HX were significantly increased in effluent venous blood but the washout was enhanced in the L-group during the initial reperfusion phase. BE was significantly higher in the L-group both before and after TR whereas pH and potassium washout was comparable between the groups. No systemic effects on platelets were detected after tourniquet release but ADP-agg. in effluent venous blood was attenuated in 6 out of 8 patients in the L-group (NS). It is concluded that HX and X are generated during leg ischemia. Regional intravenous lidocaine, most probably through a vasodilatory mechanism and inhibition of white blood cell activation, may attenuate non-reflow phenomena and thereby exert beneficial effects on post-ischemic recovery by enhancing post-ischemic tissue reperfusion.

Forty adult patients undergoing elective surgery, anaesthetized with diazepam, alfentanil and nitrous oxide in oxygen, and paralysed with atracurium were given flumazenil or placebo i.v. in a double-blind randomized study to assess the efficacy of flumazenil. Awake state, heart rate, arterial pressure, rate of ventilation and arterial blood-gas values were measured at 0, 5, 30, 120 and 240 min after administration of flumazenil or placebo. Flumazenil was found to antagonize the sedative effects of diazepam; there was no resedation within the time of observation. There were no intergroup differences in any of the other measured variables. A median dose of diazepam 0.33 mg kg-1 during surgery lasting a median of 98 min was antagonized by a median dose of flumazenil 0.35 mg. No side effects related to flumazenil were observed.