Verhaar Nicole, Hoppe Susanne, Grages Anna Marei, Hansen Kathrin, Neudeck Stephan, Kästner Sabine, Mazzuoli-Weber Gemma
Clinic for Horses, University of Veterinary Medicine Hannover, 30559 Hannover, Germany.
Institute for Physiology and Cell Biology, University of Veterinary Medicine Hannover, 30173 Hannover, Germany.
Animals (Basel). 2023 Mar 10;13(6):1021. doi: 10.3390/ani13061021.
α2 agonists are frequently used in horses with colic, even though they have been shown to inhibit gastrointestinal motility. The aim of this study was to determine the effect of dexmedetomidine on small intestinal in vitro contractility during different phases of ischaemia. Experimental segmental jejunal ischaemia was induced in 12 horses under general anaesthesia, and intestinal samples were taken pre-ischaemia and following ischaemia and reperfusion. Spontaneous and electrically evoked contractile activity of the circular and longitudinal smooth muscles were determined in each sample with and without the addition of dexmedetomidine. During a second experiment, tetrodotoxin was added to determine if the effect was neurogenic. We found that the circular smooth muscle (CSM) contractility was not affected by ischaemia, whereas the longitudinal smooth muscle (LSM) showed an increase in both spontaneous and induced contractile activity. The addition of dexmedetomidine caused a decrease in the spontaneous contractile activity of CSM, but an increase in that of LSM, which was not mediated by the enteric nervous system. During ischaemia, dexmedetomidine also mildly increased the electrically induced contractile activity in LSM. These results may indicate a stimulatory effect of dexmedetomidine on small intestinal contractility. However, the influence of dexmedetomidine administration on intestinal motility in vivo needs to be further investigated.
α2激动剂常用于患有绞痛的马匹,尽管已证明它们会抑制胃肠蠕动。本研究的目的是确定右美托咪定在不同缺血阶段对小肠体外收缩性的影响。在全身麻醉下对12匹马进行实验性节段性空肠缺血,并在缺血前以及缺血和再灌注后采集肠样本。在添加和不添加右美托咪定的情况下,测定每个样本中环行和纵行平滑肌的自发和电诱发收缩活性。在第二个实验中,添加河豚毒素以确定该作用是否为神经源性。我们发现,缺血对环行平滑肌(CSM)的收缩性没有影响,而纵行平滑肌(LSM)的自发和诱发收缩活性均增加。添加右美托咪定导致CSM的自发收缩活性降低,但LSM的自发收缩活性增加,且该作用不是由肠神经系统介导的。在缺血期间,右美托咪定还轻度增加了LSM的电诱发收缩活性。这些结果可能表明右美托咪定对小肠收缩性有刺激作用。然而,右美托咪定给药对体内肠道蠕动的影响仍需进一步研究。