Abstract
BackgroundSepsis 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 sepsis-induced ileus.MethodsSedative/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.Results40 mg·kg− 1propofol 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.ConclusionsDeep 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.
Highlights
Sepsis often accompanies gastrointestinal motility disorder that contributes to the development of sepsis in turn
Vital signs of endotoxemic mice during sedation with propofol and dexmedetomidine Vital signs of sedative endotoxemic mice were measured for 35 mins
It revealed that there was no statistical difference between endotoxemic mice with administration of 40 mg·kg− 1 propofol and 80 μg·kg− 1 dexmedetomidine for breaths (P = 0.920), oxygen saturation (P = 0.925), and systolic pressure (P = 0.608), while heart rate decreased strikingly from 10 mins after the dexmedetomidine treatment (P < 0.0001) (Fig. 2c-f)
Summary
Sepsis often accompanies gastrointestinal motility disorder that contributes to the development of sepsis in turn. 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. Impairment of intestinal motility is an inevitable complication of sepsis and sepsis has been identified as one of the risk factors for developing the gastrointestinal (GI) motility problems [2]. Inhibition of propulsive intestinal motility predisposes to gut-derived microbial translocation, which plays a pivotal role in the development of sepsis [3]. It is suggested that a vicious circle might be created by sepsis and GI motility. In sepsis, GI motility disorder demands our ongoing attention and research
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