Purine metabolite washout and platelet aggregation at reflow after tourniquet ischemia: effect of intravenous regional lidocaine.

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.