Safety and efficacy of dexmedetomidine vs. midazolam in complex gastrointestinal endoscopy: A systematic review and meta-analysis.

OBJECTIVE: This study aims to perform a meta-analysis to evaluate the safety and efficacy of dexmedetomidine versus midazolam for complex digestive endoscopy procedures, with the goal of offering comprehensive clinical evidence. METHODS: Following predefined inclusion criteria, five databases were systematically searched, with a focus on identifying randomized controlled trials (RCTs) that compared the administration of dexmedetomidine and midazolam during complex digestive endoscopy procedures. The statistical software Stata 15.1 was employed for meticulous data analysis. RESULTS: Sixteen RCTs were encompassed, involving a total of 1218 patients. In comparison to the midazolam group, dexmedetomidine administration was associated with a reduced risk of respiratory depression (RR=0.25, 95 %CI: 0.11-0.56) and hypoxemia (RR=0.22, 95 %CI: 0.12-0.39). Additionally, the dexmedetomidine group exhibited lower incidence rates of choking (RR=0.27, 95 %CI: 0.16-0.47), physical movement (RR=0.16, 95 %CI: 0.09-0.27), and postoperative nausea and vomiting (RR=0.56,95 %CI: 0.34-0.92). Patients and endoscopists in the dexmedetomidine group reported higher levels of satisfaction (patient satisfaction: SMD=0.73, 95 %CI: 0.26-1.21; endoscopist satisfaction: SMD=0.84, 95 %CI: 0.24-1.44). The incidence of hypotension and anesthesia recovery time did not significantly differ between the two groups (hypotension: RR=1.73,95 %CI:0.94-3.20; anesthesia recovery time: SMD=0.02, 95 %Cl: 0.44-0.49). It is noteworthy that the administration of dexmedetomidine was associated with a significant increase in the incidence of bradycardia in patients. CONCLUSION: Compared to midazolam, dexmedetomidine exhibits a favorable safety profile for use in complex gastrointestinal endoscopy by significantly reducing the risk of respiratory depression and hypoxemia. Despite this, dexmedetomidine is associated with a higher incidence of bradycardia. These findings underscore the need for further research through larger, multi-center studies to thoroughly investigate dexmedetomidine's safety and efficacy.

Noradrenergic activity regulated dexamethasone-induced increase of 5-HT3 receptor-mediated glutamate release in the rat's prelimbic cortex.

Stress hormone, glutamatergic system, serotonergic system and the noradrenergic system are involved in depressive disorders. However, the relationship among these is still unclear. The present study examined the effect of dexamethasone (DEX) on the presynaptic glutamate release of synaptosomes from the rat's prelimbic cortex by using biochemical methods combined with pharmacological approaches. The results showed that dexamethasone increased the glutamate release of synaptosomes in a dose-dependent manner. The concentration-response relationship of this effect of DEX was inverse U-shaped with a maximum at 3 µm. Further study showed that glucocorticoid receptor (GR) antagonist and GR siRNA had no effect on the DEX-induced glutamate release but 5-HT3 receptor antagonist could block the DEX-induced glutamate release which suggested that DEX produced the increased effect on the glutamate release not by GR, but through the activation of the 5-HT3 receptors which led to the influx of extrasynaptosomal Ca²âº. Moreover, ß3 adrenergic receptor agonist could block the DEX-induced glutamate release. This result suggested that the effect of DEX on the glutamate release could be regulated by noradrenergic system. The mechanism study showed that ß(3) adrenergic receptors regulated the DEX-induced glutamate release via Gs protein-adenylate cyclase (AC)-protein kinase A (PKA) signal transduction pathway.