Effect of sedation with dexmedetomidine or propofol on gastrointestinal motility in lipopolysaccharide-induced endotoxemic mice

Abstract

Background: Sepsis often accompanies gastrointestinal motility disorder that contributes to the development of sepsis in turn. Propofol and dexmedetomidine, as widely used sedatives in patients with sepsis, are likely to depress gastrointestinal peristalsis. We queried whether propofol or dexmedetomidine, at sedative doses, aggravated sepsisinduced ileus. Methods: Sedative/Anesthetic Scores and vital signs of lipopolysaccharide (LPS)-induced endotoxemic mice were measured during sedation with propofol or dexmedetomidine. Endotoxemic mice were divided into 10% fat emulsion, propofol, saline, and dexmedetomidine group. The gastric emptying, small intestinal transit, tests of colonic motility, gastrointestinal transit and whole gut transit were evaluated at 15 mins and 24 h after intraperitoneal injection of sedatives/vehicles respectively. Results: 40 mg•kg − 1 propofol and 80 μg•kg − 1 dexmedetomidine induced a similar depth of sedation with comparable vital signs except that dexmedetomidine strikingly decreased heart rate in endotoxemic mice. Dexmedetomidine markedly inhibited gastric emptying (P = 0.006), small intestinal transit (P = 0.006), colonic transit (P = 0.0006), gastrointestinal transit (P = 0.0001) and the whole gut transit (P = 0.034) compared with the vehicle, whereas propofol showed no depression on all parts of gastrointestinal motility 15 mins after administration. The inhibitive effects of dexmedetomidine in these tests vanished 24 h after the administration. Conclusions: Deep sedation with dexmedetomidine, but not propofol, significantly inhibited gastrointestinal peristalsis in endotoxemic mice while the inhibitory effect disappeared 24 h after sedation. These data suggested that both propofol and dexmedetomidine could be applied in septic patients while dexmedetomidine should be used cautiously in patients with cardiac disease or ileus.

Impact of intravenous dexmedetomidine on gastrointestinal function recovery after laparoscopic hysteromyomectomy: a randomized clinical trial

“…Compared with normal saline, dexmedetomidine 1 μg kg −1 for 20 min and 0.7 μg kg −1 h −1 for 190 min significantly inhibited gastric emptying and gastrointestinal transport in healthy subjects 49 . Studies in mice have shown that dexmedetomidine can inhibit gastrointestinal function in septic shock mice through Ca 2+ response on intestinal glial cells 50 , 51 . One study suggested that dexmedetomidine does not affect the intestinal function of patients undergoing abdominal hysterectomy 17 .…”

Evaluation of the effect of different sedative doses of dexmedetomidine on the intestinal motility in clinically healthy donkeys (Equus asinus)

“…The effect of different doses of dexmedetomidine on gastrointestinal motility was consistent across all donkeys at 90 minutes. Clonidine and dexmedetomidine are alpha 2 adrenoceptor agonists that induce sedation, reduce anesthetic and analgesic doses, and improve peri-operative hemodynamic balance [ 32 ]. Dexmedetomidine, unlike donkeys, inhibits gastric, small bowel, and colonic motility in animal and human studies [ 32 , 33 ].…”

Risk factors for early enteral nutrition feeding intolerance in neurocritical patients: A prospective case-control study

“…Combined sedation not only ensures the sedative and analgesic effect and reduces the inhibitory effect on the respiratory system but also promotes the recovery of cognitive function of patients. On the other hand, deep sedation can inhibit gastrointestinal functions [32,33]. In this study, the results indicated that the incidence of feeding intolerance in patients with RASS score ≤ -3 was 2.478 times higher than in patients with RASS score > -3.…”