Succinylcholine-induced Hyperkalemia and Beyond

Abstract

The mechanism of succinylcholine-induced hyperkalemia was studied in three lesions affecting canine gastrocnemius muscle. Dogs were treated for 1 month before study: 10 with normal activity, 5 with unilateral sciatic nerve section, active on 3 legs, 5 with unilateral cast immobilization of a hind limb and pelvis, active on 3 legs, and 7 inactive with T6 section of the spinal cord. Succinylcholine responses were determined during thiopental―ha lothane (mean expired halothane 1.0 ± 0.2%) endotracheal anesthesia with arterial carbon dioxide tension of 38—42 mmHg, arterial oxygen tension of 100—120 mmHg, and muscle and body temperatures maintained at 37° ± 0.2°C. The investigators isolated and collected the venous drainage of gastrocnemius muscle and measured its total blood flow. Muscle potassium release and oxygen consumption were calculated as blood flow x (arterial content — venous content). Succinylcholine-induced gastrocnemius potassium release was greatest after both sciatic and cord section; oxygen consumption was increased in parallel. Disuse atrophy of one leg slightly increased both values but was insufficient to produce systemic hyperkalemia. Reuptake of potassium followed succinylcholine-induced release. Given before succinylcholine, modest doses of gallamine slightly modified the release of potassium, and total paralysis by gallamine blocked it.