Efficacy of Electroacupuncture Combined with Tropisetron in Treating Carboprost Tromethamine-Induced Nausea and Vomiting during Cesarean Section under Lumbar Anesthesia.

OBJECTIVE: We evaluated the efficacy of electroacupuncture combined with tropisetron in treating carboprost tromethamine-induced nausea and vomiting during cesarean section under lumbar anesthesia. METHODS: A total of 264 patients aged 22-40 years were enrolled, who received carboprost tromethamine and suffered nausea and vomiting during cesarean section under lumbar anesthesia. The patients were divided randomly into the control group, electroacupuncture group, tropisetron group, and electroacupuncture + tropisetron group. RESULTS: Compared to the control group, the nausea and vomiting scores decreased at T3 in both the electroacupuncture and electroacupuncture + tropisetron groups, and decreased at T4 in the electroacupuncture group, tropisetron group, and electroacupuncture + tropisetron group; the motilin, gastrin, and 5-hydroxytryptamine (5-HT) levels decreased at T5 in the other 3 groups. Compared to the electroacupuncture + tropisetron group, the nausea and vomiting scores increased at T3 in the control and tropisetron groups, and increased at T4 in the other 3 groups; the motilin, gastrin, and 5-HT levels increased at T5. CONCLUSIONS: Our study suggested that electroacupuncture combined with tropisetron could effectively relieve carboprost tromethamine-induced nausea and vomiting during cesarean section under lumbar anesthesia. The effect was better than its single application, and the reduced 5-HT, motilin, and gastrin levels might be involved in the underlying mechanism.

Propofol can suppress renal ischemia-reperfusion injury through the activation of PI3K/AKT/mTOR signal pathway.

INTRODUCTION: Renal ischemia/reperfusion injury (IRI) remains one of the most diseases in clinic. The purpose of this study was to investigate the potential role and mechanism of propofol in protecting mice kidney from IRI. METHODS: Renal I/R model was established in C57/BL6 mice by clamping bilateral renal pedicles for 35 min. The mice were randomly divided into four groups: sham group, IR group, IR + Propofol group, and IR + Propofol+LY294002 group. Histological assessment of kidney was conducted by HE staining and the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) of each group were measured. Expressions of inflammatory factors (IL-6, TNF-α) were detected by qRT-PCR and immunoblotting. The expression levels of cleaved Caspasse-3, PI3K, Akt, p-Akt, mTOR, and p-mTOR within renal tissue samples were measured by Western Blot. RESULTS: The levels BUN, Cr and morphological damage score increased significantly after renal IRI. However, such changes could be prevented by propofol. Besides, IRI reduced renal expressions of PI3K, p-Akt, p-mTOR, and increased the levels of IL-6, TNF-α，cl-caspase-3 in kidney, After propofol treatment, these changes were significantly alleviated, but the use of PI3K inhibitor LY294002 could reverse the effects of propofol. CONCLUSION: Propofol can protect renal IRI partially by reducing apoptosis and release of inflammatory cytokines, which is possibly involved in the modulation of the PI3K/AKT/mTOR signaling pathway. Our data suggested that propofol may play certain positive roles in protecting the kidney from IRI.