Marathe P H, Haschke R H, Slattery J T, Zucker J R, Pavlin E G
Department of Anesthesiology, University of Washington, Seattle 98195.
Anesthesiology. 1989 Apr;70(4):654-9. doi: 10.1097/00000542-198904000-00019.
Thermal injury causes systemic changes that result in altered sensitivity to many drugs including nondepolarizing muscle relaxants. In an effort to identify the mechanism(s) responsible for the resistance to nondepolarizing muscle relaxants, the density of acetylcholine receptors (AChR) and the activity of acetylcholinesterase (AChE) were determined in rats following a 30% total body surface thermal injury at a time when resistance to atracurium is maximum. AChR density in gastrocnemius and diaphragm was unchanged by thermal injury. Furthermore, the ratio of junctional to extrajunctional AChR in diaphragm was unaltered. Total AChE activity was unchanged in thermally injured rats compared with that in sham-injured animals. Separation of the molecular forms of AChE by sucrose gradient centrifugation also showed no changes in the relative proportions of these species. The mechanism of resistance to nondepolarizing muscle relaxants does not appear to be explained by changes in AChR number or changes in the activity of AChE.
热损伤会引起全身变化，导致对包括非去极化肌松药在内的许多药物的敏感性改变。为了确定对非去极化肌松药产生耐药性的机制，在对阿曲库铵的耐药性达到最大时，测定了30%体表面积热损伤大鼠的乙酰胆碱受体（AChR）密度和乙酰胆碱酯酶（AChE）活性。热损伤并未改变腓肠肌和膈肌中的AChR密度。此外，膈肌中接头处与接头外AChR的比例未发生改变。与假手术动物相比，热损伤大鼠的总AChE活性没有变化。通过蔗糖梯度离心分离AChE的分子形式，也显示这些形式的相对比例没有变化。对非去极化肌松药产生耐药性的机制似乎无法用AChR数量的变化或AChE活性的变化来解释。
