Sakura S, Chan V W, Ciriales R, Drasner K
Department of Anesthesia, University of California, San Francisco.
Anesthesiology. 1995 Jan;82(1):236-40. doi: 10.1097/00000542-199501000-00028.
Recent reports of major and minor neurologic sequelae after spinal anesthesia have generated concern regarding the safety of some currently used intrathecal agents. The role of glucose, if any, in neurotoxic injury associated with spinal anesthesia is not known. The current experiments sought to determine whether the presence of 7.5% glucose alters the neurotoxicity of intrathecally administered 5% lidocaine.
Two experiments were performed. First, 48 rats were implanted with an intrathecal catheter and randomly divided into eight equal groups. Each animal received a single intrathecal infusion of 5% lidocaine (groups P1-P4) or 5% lidocaine with 7.5% glucose (G1-G4) for 0.5, 1, 2, or 4 h at a rate of 1 microliter/min. Sensory function was assessed using the tail-flick test; a deficit was defined as a complete lack of response to the heat stimulus at the proximal, mid or distal portion of the tail persisting 4 days after the infusion. In the second experiment, 60 rats were randomly divided into two groups to receive a 1-h intrathecal infusion of 5% lidocaine or 5% lidocaine with 7.5% glucose. Animals were evaluated for increase in the latency of the tail-flick reflex 4 days after infusion.
In the first experiment, the two lidocaine solutions produced similar dose-dependent loss of sensory function. In the second experiment, the two solutions induced similar alterations in tail-flick latency.
The presence of 7.5% glucose does not affect the potential of intrathecally administered 5% lidocaine to induce sensory impairment. These findings provide further support for the hypothesis that recent injuries after spinal anesthesia resulted from a direct neurotoxic effect of the local anesthetic.
近期有关脊髓麻醉后出现严重和轻微神经后遗症的报道引发了人们对一些当前使用的鞘内注射药物安全性的关注。葡萄糖(若有)在与脊髓麻醉相关的神经毒性损伤中的作用尚不清楚。当前的实验旨在确定7.5%葡萄糖的存在是否会改变鞘内注射5%利多卡因的神经毒性。
进行了两项实验。首先,给48只大鼠植入鞘内导管,并随机分为八组。每只动物以1微升/分钟的速率接受单次鞘内输注5%利多卡因(P1 - P4组)或含7.5%葡萄糖的5%利多卡因(G1 - G4组),持续0.5、1、2或4小时。使用甩尾试验评估感觉功能;缺陷定义为在输注后4天,尾巴近端、中部或远端对热刺激完全无反应。在第二项实验中,将60只大鼠随机分为两组,接受1小时的鞘内输注5%利多卡因或含7.5%葡萄糖的5%利多卡因。在输注后4天评估动物甩尾反射潜伏期的增加情况。
在第一项实验中,两种利多卡因溶液产生了相似的剂量依赖性感觉功能丧失。在第二项实验中,两种溶液诱导的甩尾潜伏期变化相似。
7.5%葡萄糖的存在并不影响鞘内注射5%利多卡因诱导感觉障碍的可能性。这些发现为脊髓麻醉后近期损伤是由局部麻醉药的直接神经毒性作用所致这一假说提供了进一步支持。