作者: Gerald A. Gronert , David S. Warner
DOI: 10.1097/ALN.0B013E3181C0AD7C
关键词: Medicine 、 Anesthesia 、 Paralysis 、 Sciatic nerve 、 Halothane 、 Hindlimb 、 Potassium 、 Gastrocnemius muscle 、 Blood flow 、 Hyperkalemia
摘要: 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 unilateral sciatic nerve section, active on 3 legs, cast immobilization a hind limb and pelvis, 7 inactive T6 section the spinal cord. Succinylcholine responses determined during thiopental―ha lothane (mean expired halothane 1.0 ± 0.2%) endotracheal anesthesia arterial carbon dioxide tension 38—42 mmHg, oxygen 100—120 muscle body temperatures maintained at 37° 0.2°C. investigators isolated collected venous drainage measured its total blood flow. Muscle potassium release consumption calculated as flow x (arterial content — content). Succinylcholine-induced greatest after both cord section; increased parallel. Disuse atrophy one leg slightly values but insufficient to produce systemic hyperkalemia. Reuptake followed release. Given succinylcholine, modest doses gallamine modified potassium, paralysis by blocked it.