Background:To assess the effect of dexmedetomidine added to ropivaccaine on the onset and duration of sensory block, as well as postoperative analgesia during caudal anesthesia in patients undergoing hemorrhoidectomy.Methods:Fifty adult patients scheduled for hemorrhoidectomy were divided into 2 groups. The group R received caudal anesthesia using 18 mL 0.3% ropivacaine plus 2 mL normal saline. The group RD received 18 mL 0.3% ropivacaine plus 2 mL 1 μg/kg dexmedetomidine. Heart rate, mean blood pressure, onset time and duration of sensory block, and duration of analgesia were observed.Results:The onset time of sensory block was shortened (9.2 ± 1.3 vs 7.2 ± 1.2), and the duration of sensory block (3.0 ± 0.7 vs 3.8 ± 0.8) and duration of analgesia (3.9 ± 0.7 vs 5.3 ± 0.8) were prolonged in group RD compared with group R (P < .05). The heart rate and the mean blood pressure were also lower in the group RD compared with group R at each observation time points, except the baseline (P < .05). No bradycardia or hypotension was reported.Conclusion:Dexmedetomidine as an adjuvant to ropivacaine prolonged the duration of caudal block and improved postoperative analgesia without significant side effects in adult patients undergoing hemorrhoidectomy.
Background. Propofol (PPF) has been shown in studies to cause cognitive impairment and neuronal cell death in developing animals. PPF has been demonstrated to decrease the expression of microRNA-17-5p (miR-17-5p) in a recent study. Nonetheless, the function of miR-17-5p in PPF-induced neurotoxicity and related mechanisms is uncharacterized. Methods. After the induction of neurotoxicity by treating the SH-SY5Y cells with PPF, qRT-PCR was conducted to evaluate the level of miR-17-5p. Using MTT and flow cytometry, cell viability and apoptosis rate were assessed, respectively. Interaction between miR-17-5p and BCL2 like 11 was (BCL2L11) studied using a Luciferase reporter assay. With the help of western blot analysis, we determined the level of proteins of apoptosis-related genes and autophagy-related markers. Results. In SH-SY5Y cells, PPF treatment induced neurotoxicity and downregulated miR-17-5p expression. In SH-SY5Y cells post-PPF exposure, overexpression of miR-17-5p increased cell viability and decreased apoptosis. Consistently, miR-17-5p mimics mitigated PPF-generated autophagy via inhibition of Atg5, Beclin1, and LC3II/I level and elevation of p62 protein expression. In addition, BCL2L11, which was highly expressed in PPF-treated SH-SY5Y cells, was directly targeted by miR-17-5p. Further, in PPF-treated SH-SY5Y cells, overexpressed BCL2L11 counteracted the suppressing behavior of miR-17-5p elevation on PPF-induced apoptosis. Conclusion. Overexpressed miR-17-5p alleviates PPF exposure-induced neurotoxicity and autophagy in SH-SY5Y cells via binding to BCL2L11, suggesting the possibility that miR-17-5p can serve as a candidate in the treatment of neurotoxicity (caused by PPF).
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