Diego Duarte Varela

Endotoxemia is a major contributor to gastrointestinal hypomotility and postoperative ileus in horses. This study investigated whether oral mosapride retained prokinetic activity during acute lipopolysaccharide (LPS)-induced endotoxemia. Seven healthy adult horses were enrolled in a randomized, blinded, three-period crossover trial and received LPS alone, mosapride alone (MOSA), or LPS plus mosapride (LPS + MOSA), with a 14-day washout interval between periods. Mosapride was administered orally at 2 mg/kg, whereas endotoxemia was induced by an intravenous infusion of Escherichia coli O55:B5 LPS (0.03 µg/kg) over 30 min. Clinical variables, hematologic parameters, abdominal auscultation, and transabdominal ultrasonography were assessed from baseline to 6 h. LPS induced tachycardia, hyperthermia, leukocyte alterations, marked gastrointestinal hypomotility, gastric distension, and increased intestinal wall thickness. Mosapride alone increased gastrointestinal motility without clinically relevant abnormalities. During endotoxemia, mosapride partially restored gastrointestinal motility, reduced intestinal wall thickening and gastric distension, and was associated with a less pronounced hematologic inflammatory response than LPS alone. These findings indicate that oral mosapride retains clinically relevant prokinetic activity during acute experimental endotoxemia and support further investigation of its use as an adjunctive treatment for inflammation-associated gastrointestinal hypomotility in horses.

The present study involved seven horses in a randomized crossover clinical trial to evaluate the effect of lidocaine on horses with induced endotoxemia. Horses received intravenous lidocaine (1.5 mg/kg bolus, followed by 0.05 mg/kg bwt/min) or placebo (0.9% sodium chloride at the same manner) one hour before LPS administration (0.03 μg/kg, IV infusion over 30 min). We monitored clinic and hematologic parameters, abdominal auscultation, ultrasound, and pain over time. No relevant clinical differences existed between treatments regarding peristalsis, abdominal pain, or any other parameters before and after endotoxemia induction. These findings do not support the clinical use of lidocaine to mitigate abdominal pain and intestinal hypomotility promoted by endotoxemia in horses.