Dwinell M B, Bass P, Oaks J A
Department of Comparative Biosciences, School of Veterinary Medicine, University of Wisconsin, Madison 53706, USA.
J Parasitol. 1995 Dec;81(6):979-84.
Hymenolepis diminuta-associated alterations in rat intestinal myoelectric patterns are abolished following therapeutic administration of the anthelmintic praziquantel (PZQ). Host intestinal smooth muscle myoelectric patterns, reflecting smooth muscle contractility and intestinal phasic motility, were recorded using in vivo serosal electrodes, surgically implanted on the duodenum, jejunum, and ileum. Repeated electromyographic recording from unrestrained and unanesthetized rats began 5 days after electrode implantation surgery. Three initial control recordings from each rat confirmed the appearance of normal intestinal myoelectric patterns, characterized by the interdigestive migrating myoelectric complex (MMC). All animals were subsequently infected with H. diminuta and myoelectric recordings beginning after day 8 postinfection confirmed the appearance of diminished frequency of the MMC and 2 nonmigrating myoelectric patterns, i.e., repetitive bursts of action potentials and sustained spike potentials. PZQ was used to remove the tapeworms from rats 12 days after Hymenolepis diminuta infection, as intestinal myoelectric changes become maximal at this time in tapeworm-infected rats. PZQ administered to uninfected rats at either of 2 dose levels did not affect host interdigestive myoelectric activity. After removal of the parasite with PZQ, electromyographic recordings indicated a return to normal uninfected electrical patterns within 24 hr of drug treatment. We have demonstrated that the presence of Hymenolepis diminuta is necessary to induce and maintain abnormal intestinal myoelectric patterns. The altered motor properties of tapeworm-infected rat intestine and the rapid reconversion to preinfection myoelectric patterns provides a new and unique model to examine the regulatory mechanisms of intestinal motility and its control by luminal parasites.
给予驱虫药吡喹酮（PZQ）进行治疗后，微小膜壳绦虫引起的大鼠肠道肌电模式改变被消除。使用手术植入十二指肠、空肠和回肠的体内浆膜电极记录宿主肠道平滑肌肌电模式，该模式反映平滑肌收缩力和肠道阶段性运动。在电极植入手术后5天开始对未受约束和未麻醉的大鼠进行重复肌电图记录。每只大鼠的三次初始对照记录证实了正常肠道肌电模式的出现，其特征为消化间期移行性肌电复合波（MMC）。随后所有动物均感染微小膜壳绦虫，感染后第8天开始的肌电记录证实MMC频率降低以及出现两种非移行性肌电模式，即动作电位的重复爆发和持续的棘波电位。在微小膜壳绦虫感染12天后，使用PZQ清除大鼠体内的绦虫，因为此时绦虫感染大鼠的肠道肌电变化达到最大。给予未感染大鼠两种剂量水平之一的PZQ均不影响宿主消化间期肌电活动。用PZQ清除寄生虫后，肌电图记录表明在药物治疗后24小时内恢复到未感染时的正常电模式。我们已经证明，微小膜壳绦虫的存在是诱导和维持异常肠道肌电模式所必需的。绦虫感染大鼠肠道运动特性的改变以及迅速恢复到感染前的肌电模式为研究肠道运动的调节机制及其受腔内寄生虫控制提供了一个新的独特模型。
