Department of Physiology, University of Veterinary Medicine, Bischofsholer Damm 15, D-30173 Hannover, Germany.
Vet J. 2013 Oct;198(1):170-5. doi: 10.1016/j.tvjl.2013.07.027. Epub 2013 Aug 22.
The purpose of the study was to compare the contractility-enhancing effects of lidocaine in equine jejunal circular (CSM) and longitudinal smooth muscle (LSM) in vitro. In previous studies, more pronounced effects of lidocaine were observed in ischaemia-reperfusion (IR) injured smooth muscle. Therefore in this study, effects were examined in both non-injured control tissues and tissues challenged by a defined, artificial IR injury. Isometric contractile performance of CSM and LSM, assessed by frequency (F), amplitude (A) and mean active force (MAF) of contractions, was defined as contractility. LSM featured lower basic contractility compared to CSM. Lidocaine provoked contractility-enhancing effects in both smooth muscle layers, but except for F at high lidocaine concentrations, contractility of LSM remained lower throughout the trial. Additionally, higher lidocaine concentrations were required to cause significant effects in LSM. No differences were observed in contractility of control and IR injured smooth muscle, but higher lidocaine concentrations were needed to provoke effects in IR injured smooth muscle. In contrast to CSM, contractility of LSM did not decrease at comparably high lidocaine concentrations. Differences in basic contractility of CSM and LSM might be explained by physiologically lower activity of LSM per se or by a thinner LSM layer with fewer smooth muscle cells taking part in contractions. The smaller thickness of the LSM layer may also contribute to persisting discrepancies in contractility following lidocaine application. Additionally, variations in lidocaine concentrations necessary for inducing significant effects could result from differences in the molecular structure of CSM and LSM cells.
本研究旨在比较利多卡因对马空肠环形(CSM)和纵向平滑肌(LSM)体外收缩性的增强作用。在以前的研究中,在缺血再灌注(IR)损伤的平滑肌中观察到利多卡因更明显的作用。因此,在这项研究中,在未受伤的对照组织和受到特定人工 IR 损伤的组织中检查了作用。通过收缩频率(F)、幅度(A)和平均主动力(MAF)评估 CSM 和 LSM 的等长收缩性能,定义为收缩性。与 CSM 相比,LSM 的基础收缩性较低。利多卡因在两种平滑肌层中均引起收缩性增强作用,但除高利多卡因浓度下的 F 外,整个试验中 LSM 的收缩性仍较低。此外,需要更高的利多卡因浓度才能引起 LSM 产生显著作用。在对照和 IR 损伤的平滑肌的收缩性中未观察到差异,但需要更高的利多卡因浓度才能在 IR 损伤的平滑肌中引起作用。与 CSM 不同,LSM 的收缩性在可比的高利多卡因浓度下不会降低。CSM 和 LSM 的基础收缩性差异可能是由于 LSM 本身的生理活性较低,或者由于参与收缩的平滑肌细胞较少的 LSM 层较薄所致。LSM 层的较小厚度也可能导致在利多卡因应用后持续存在收缩性差异。此外,引起显著作用所需的利多卡因浓度的变化可能是由于 CSM 和 LSM 细胞的分子结构不同所致。