In order to explore more ideal intravenous anesthesia drug in clinical practice, the analgesic effect of remazolam combined with etomidate in painless gastroenteroscopy and its effect on stress response is investigated. A total of 100 patients are selected for the gastric disease screening, and they are randomly divided into the single-drug group and composite group, with 50 cases in each group. Etomidate, mazzolone, and etomidate are used to anesthetize the patients, and then, the effects of different solutions on analgesia, sedation, and stress response are compared and analyzed, and the adverse reactions are improved. The etomidate and red horse azole shimron composite etomidate anesthesia were applied, and the comparative analysis of different solutions of analgesic, sedative effect, and response to stress is conducted. Then, the improvement of adverse reactions is analyzed. The experimental results demonstrate that remazolam combined with etomidate anesthesia can reduce the level of pain mediators and enhance the analgesia and sedation effect. Meanwhile, combined anesthesia can reduce the stress response and adverse reactions of patients and shorten the examination period effectively.
Sevoflurane (SEV) is a commonly used anesthetic in pediatric surgery. Recent studies reported that repeated use of SEV contributes to cognitive impairment. Engeletin has been discovered to exert anti‐inflammatory effects in various diseases. However, the detailed roles and mechanisms of engeletin in SEV‐induced cognitive dysfunction of neonatal mice remain unclear. In this study, C57BL/6 neonatal mice were randomly divided into Ctrl, SEV, SEV + Engeletin (10 mg /kg), SEV + Engeletin (20 mg/kg), and SEV + Engeletin (40 mg/kg) groups. The Morris water maze (MWM) test suggested that engeletin treatment significantly improved SEV‐induced cognitive impairment in neonatal mice. Employing ELISA and Nissl staining analysis, engeletin reduced neuroinflammation and loss of nerve cells caused by SEV, respectively. The treatment of engeletin dramatically suppressed the activation of microglia and apoptosis induced by SEV in the hippocampus of neonatal mice. Furthermore, the inhibition of PPAR‐γ obviously reversed the abovementioned effects of engeletin in the hippocampus of newborn mice. In conclusion, this study verified that engeletin notably ameliorated SEV‐induced cognitive deficiencies in neonatal mice at least partially by mediating the expression of PPAR‐γ.
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