In vitro effects of erythromycin, lidocaine, and metoclopramide on smooth muscle from the pyloric antrum, proximal portion of the duodenum, and middle portion of the jejunum of horses

Abstract

Regional differences in responses to erythromycin, lidocaine, and metoclopramide were evident in the gastrointestinal tract of horses. Metoclopramide increased CA in all tissues used, whereas erythromycin inhibited CA in circular smooth muscle but stimulated CA in longitudinal smooth muscle from the PA. Inhibition is caused by stimulation of inhibitory nerves and is mediated, in part, by nitric oxide and vasoactive intestinal peptide.

In vitro analysed effects of two different in vivo administered lidocaine dosageson the equine jejunal smooth muscle challenged by an ischemia-reperfusion-injury-model (IRIM)

“…However, the same dosage of lidocaine (10 -4 mmol/L) used in this experiment was also described as effective dose in vitro by Nieto et al (2000). This discrepancy between in vivo and in vitro effective dosages might be based on certain biochemical features of lidocaine but cannot be explained satisfactorily yet.…”

“…The present study presents a sequel study to the basic research approaches by Nieto et al 2000 andGuschlbauer et al 2010a to improve the knowledge on lidocaine prokinetic effects in intestinal smooth muscle of horses. The present results are proving the hypothesis that a higher initial dose of lidocaine during IR in vivo could change and slightly improve but not impair the contractility of jejunal smooth muscle in vitro.…”

“…Furthermore, four KHB strips (n = 4) were prepared per horse and were mounted in organ baths without supplementation of lidocaine. The initial tension of all muscle strips was adjusted to 2 g, because preliminary studies showed that 2 g of tension resulted in optimal muscle length for maximal isometric force development in the jejunum (Nieto et al 2000). To study the effects of lidocaine on smooth muscle cells and interstitial cells of Cajal (ICC) only, the tissue strips in the organ bath were treated with tetrodotoxin (TTX 1 mol/L) in order to deactivate the enteric nervous system neurons.…”

“…Besides its local anesthetic effects, lidocaine is used for antiarrhythmic and antiepileptic treatment (Löscher et al 2003). Furthermore, lidocaine is known to have protective and/or prokinetic effects on intestinal smooth muscle (Nieto et al 2000, Guschlbauer et al 2010a) and heart muscle (Takeo et al 1989) after ischemia-reperfusion (IR) injury although the mechanism of its protective and prokinetic effects are still unclear. Administration of lidocaine significantly decrease liberation of substances from body cells such as hypoxiainduced release of creatine kinase from the intestinal smooth muscle (Guschlbauer et al 2010a) and from the heart muscle (Takeo et al 1989), and attenuates inflammatory response by decreasing the plasma concentrations of complement factors and pro-inflammatory cytokines released by inflammatory cells (Herroeder et al 2007).…”

“…Previous studies revealed that in vitro lidocaine supplementation of 25 x 10 9 ng/ml = 25 mg/L = 10 -4 mol/L is needed to improve effectively contractile activity of the equine jejunal smooth muscle (Guschlbauer et al 2010a, Nieto et al 2000. After continuous infusion of lidocaine as used in the treatment of post operative ileus (POI) (bolus of 1.3 mg/kg over 10 min.…”