Background:
The effective therapy to reduce postoperative catheter-related bladder discomfort (CRBD) remained unknown.
Objective:
We attempted to manage the systematic review and a meta-analysis to clarify the efficacy of dexmedetomidine (DEX) in potential prevention on CRBD.
Methods:
We performed the meta-analysis on randomized clinical trials (RCTs), and searched the databases from Web of Sciences, Embase and referred Cochrane Library published from October 2016 to September 2020. Data extraction was carefully conducted by 2 authors, respectively. Meta-analysis that was applied synthetically concerns the incidence and severity of CRBD and the treatment effect of DEX on CRBD.
Results:
We acquired 5 RCTs with interventions of DEX on CRBD. Meta-analysis showed DEX has significantly reduced the incidence and severity of CRBD compared with control at 0 hour (risk ratios [RR] = 0.40, 95% CI = 0.53–0.29,
P
< .01), 1 hour (RR = 0.44, 95% CI = 0.34–0.57,
P
< .01), and 2 hours (RR = 0.43, 95% CI = 0.32–0.58,
P
< .01) and 6 hours (RR = 0.43, 95% CI = 0.29–0.63,
P
< .01). DEX was also associated with lower incidence of moderate to severe CRBD at 0, 1, and 6 hours after surgery. There were no significant differences in adverse events other than bradycardia, hypotension, and hypertension.
Conclusion:
The 5 RCTs showed great effectiveness in reducing the incidence and severity of the early and later postoperative CRBD. Meta-analysis showed that DEX interventions were useful in preventing the early and later postoperative CRBD without significant side effects.
Introduction: Sevoflurane acts as a gamma-aminobutyric acid subtype A receptor agonist and can induce widespread apoptosis of immature dentate granule cells in postnatal day 21 mice. The dentate granule cells of postnatal day 21 mice undergo a developmental stage when gamma-aminobutyric acid (GABA) shifts from inducing the depolarization of neurons to causing hyperpolarization. However, it is unclear whether sevoflurane induces apoptosis of immature granule cells by facilitating the depolarization or hyperpolarization of neurons.
Methods:We utilized bumetanide, an Na + -K + -2Cl − cotransporter isoform 1 (NKCC1) antagonist, to determine whether the NKCC1-mediated GABA depolarization of neurons plays a role in sevoflurane-induced neuroapoptosis. We also investigated whether sevoflurane exposure is related to long-term cognitive dysfunction in postnatal day 21 mice and explored the possible protective effects of bumetanide.Results: Bumetanide attenuated the sevoflurane-induced apoptosis of dentate granule cells in postnatal day 21 mice. Exposure to sevoflurane at postnatal day 21 mice did not affect their motor ability or anxiety level, and it had no effect on spatial learning or memory functions. However, sevoflurane exposure at postnatal day 21 impaired the pattern separation ability in the contextual fear discrimination test; bumetanide mitigated this effect of sevoflurane as well.
Conclusion:Bumetanide attenuates sevoflurane-induced apoptosis and is a promising prospect for protecting against anesthesia-induced neurotoxicity in the developing brain.
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