The perioperative use of 0.04ug/kg/h enhanced the recovery of postoperative bowel movement.
POI is a common complication after abdominal operations, and the clinical manifestations vary, including abdominal distension, nausea, vomiting, difficulty in defecation and prolonged feeding time. The causes of POI are complicated and involve many factors, including surgical trauma, activation of the inhibitory sympathetic reflex, and induction of local and systemic inflammatory mediators [2, 3].
First, the sympathetic nerve inhibits bowel movement by reducing the release of acetylcholine, and the vagus nerve stimulates bowel movement by inducing the release of acetylcholine. Nerve reflex regulation is an important physiological mechanism for postoperative control of bowel movement. Surgery, pain, gut damage and other factors, directly or indirectly activate the sympathetic nerve to inhibit postoperative bowel movement. As a highly selective α2-adrenoceptor agonist, DEX inhibits sympatholytic excitation, sedation and analgesia. It acts on α2-adrenoceptors in the central nervous system to reduce sympathetic tone . Hence, after the use of DEX, the activated sympathetic nerve was downregulated, and the vagus nerve was relatively excited; as a result, bowel movements were facilitated.
Second, postoperative pain was relieved by perioperative use of DEX [7 ~ 9]. Although opioids are a priority for postoperative pain, they are unfavorable because they inhibit gastrointestinal motility and aggravating POI [10, 11]. In our study, laparoscopic surgery relieved postoperative pain compared with open surgery.. Although the total volumes of opioid drugs were not different among the three groups, postoperative pain with rest and movement was significantly relieved by the combined use of DEX. Effective pain relief contributed to alleviating POI by allowing for postoperative activities earlier.
Third, the influence of gut damage on POI was excluded by laparoscopic nephrectomy. Laparoscopic surgery can reduce surgical trauma and weaken the immune response compared with open surgery, reducing the time for flatulence and shorting the time to resume a soft diet after surgery and decreasing the length of the hospital stay [12 ~ 14]. Visualizing laparoscopic surgery and pneumoperitoneum induction can lead to sympathetic nerve activation [15, 16]. In addition, CO2 pneumoperitoneum can induce hypercarbia, which can directly or indirectly stimulate the sympathetic nervous system and cause evaluated levels of catecholamine [15, 17]. Sympathetic stimulation could provide the main inhibitory force for intestinal peristalsis, while parasympathetic stimulation enhances gastrointestinal motility . DEX, as a highly selective α-2 adrenergic receptor agonist, acts on α2-adrenoceptors in the central nervous system to reduce sympathetic tone and decrease the secretion of catecholamine . It has also been proved to reduce the sympathetic effect caused sweating and abate blood pressure increased and catecholamine release caused by tremor . DEX has been proved to attenuate sympathetic activation induced by pneumoperitoneum and surgical stress . Hence, DEX could prompt postoperative bowel movement by weakening sympathetic activation. In our study the flatus times and defecation times were significantly shorter after the use of DEX. The outcomes were consistent with previous hypothesis. Between the groups D1 and D2, group D2 had shorter flatus and defecation times than group D1, although the difference was insignificantly. For patients, one hour is still important. This study provides evidence for the relief of postoperative peristalsis in patients undergoing endoscopic surgery.
When DEX was used as a bolus, the blood vessels contracted and hypertension could be seen in the first 1–3 min. It was seen but not recorded, and when used as an infusion drug, the central sympatholytic impact of DEX was the main effect [21, 22]. Developing bradycardia and hypotension (requiring treatment) were increased only when a loading dose and a maintenance dose of DEX > 0.07 µg/kg/h were given to critically ill patients.  HR and MBP were significantly lower after the loading dose of DEX without bradycardia and hypotension. DEX could decrease the plasma concentration and the release of catecholamine [6, 21, 24]. The infusion of DEX during anesthesia showed a medium decrease and fewer variations in MBP and HR [25, 26]. There was an insignificant difference among the three groups in HR and MBP, so the dose of DEX was safe for patients.
DEX, as a highly selective α-2 adrenergic receptor agonist, has the effects of leep induction, and sedation, with little respiratory inhibition [5, 27]. There were no significant differences in drowsiness, which is easily arousable, or severe respiratory depression, which was not consistent with its sedative effect to some extent [28, 29]. There were no significant differences PONV or postoperative delirium which was not consistent with the report of Song et al [30 ~ 32].
Some limitations exist in our study. First, before anesthesia induction, DEX was administered at a rate of 0.5 µg/kg for 10 minutes and then at a rate of 0.2 to 0.4 µg/kg/h during the operation. However, we were unable to determine the effect of plasma DEX concentrations on intraoperative hemodynamics because we did not measure the serum concentrations of DEX at any time point. Finally, laparoscopic nephrectomy was performed by two different surgical methods: transabdominal and retroperitoneal. Therefore, different surgical techniques might have had different effects on postoperative analgesia and the recovery of bowel movement.