Succinylcholine-induced Hyperkalemia and Beyond
نویسندگان
چکیده
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–halothane (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 (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.
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