BackgroundLaparoscopic cholecystectomy (LC) has become the ‘gold standard’ for the treatment of symptomatic gallstones. Innovative methods are being introduced, and these procedures include transgastric or transcolonic endoscopic cholecystectomy. However, before clinical implementation, instruments still need modification, and a more convenient treatment is still needed. Moreover, some gallbladders still have good functionality and cholecystectomy may be associated with various complications. The aim of this study was to evaluate the trans-gastrointestinal tract cholecystoscopy technique in the treatment of gallbladder disease without cholecystectomy.MethodEndoscopic ultrasound (EUS)-guided cholecystoduodenostomy or cholecystogastrostomy with the placement of a double-flanged fully covered metal stent was performed and endoscopic sphincterotomy (EST) was also performed during this procedure for those patients with accompanying common bile duct stones. One or two weeks later the stent was removed and an endoscope was advanced into the gallbladder via the fistula, and cholecystolithotomy or polyp resection was performed. Four weeks later gallbladder was assessed by abdominal ultrasound.ResultsEUS guided cholecystoduodenostomy (n = 3) or cholecystogastrostomy (n = 4) with double flanged mental stent deployment was successfully performed in all of 7 patients. After the procedure, fistulas had formed in each of the patients and the stents were removed. Endoscopic cholecystolithotomy(7) and polyps resection(2) were successfully performed through the fistulas. Common bile duct stones were also successfully removed in 5 patients. The ultrasound examination of the gallbladder 4 weeks later showed no stones remaining and also showed satisfactory functioning of the gallbladder.ConclusionThe EUS-guided placement of a novel metal stent is a safe and simple approach for performing an endoscopic cholecystoduodenostomy or cholecystogastrostomy, which can subsequently allow procedures to be performed for treating biliary disease, including cholecystolithotomy.
BackgroundThe effect of sevoflurane on the nervous system is controversial. As an adjuvant anesthetic, dexmedetomidine has a protective role in various nerve-injury diseases. We investigated the effect of dexmedetomidine on injury to the developing brain induced by sevoflurane anesthesia, and if autophagy and mitochondrial damage are involved in the neuroprotective effects of dexmedetomidine.MethodsPregnant rats on gestational day 20 were exposed to 3% sevoflurane for 4 hours. Saline and dexmedetomidine were injected intraperitoneally 15 minutes before exposure to sevoflurane or control gas. Bilateral hippocampi were harvested on postnatal day 1. Hippocampal morphology was observed by Nissl staining and expression of the microtubule-related protein LC3I/II, p62, Drp1, Bax, and Bcl2 were evaluated by Western blotting and immunohistochemistry.ResultsNissl staining showed that sevoflurane anesthesia during the third trimester caused neuronal damage to the hippocampi of rat pups. Western blotting and immunohistochemistry showed that pregnant rats exposed to sevoflurane during the third trimester led to pups having increased expression of LC3 and p62, suggesting that sevoflurane blocked autophagic flow in the hippocampus. Expression of Drp1 and Bax was increased after sevoflurane exposure, whereas Bcl2 expression was downregulated. All these effects were alleviated by pretreatment with dexmedetomidine.ConclusionSevoflurane exposure during the third trimester caused neurological injury to rat pups. Autophagy and abnormalities in mitochondrial dynamics were involved in this neurotoxic process and were antagonized by dexmedetomidine.
Numerous studies have demonstrated that general anesthetics might damage the nervous system, thus, the effect of general anesthetics on the developing brain has attracted much attention. Dexmedetomidine (Dex) exhibits a certain neuroprotective effect, but the mechanism is obscure. In our study, pregnant rats on gestational day 20 (G20) were exposed to 3% sevoflurane for 2 h or 4 h, and the neuronal apoptosis in hippocampal CA1 region of the offspring rats was detected by quantification of TUNEL positive cells and cleaved-caspase3 (cl-caspase3). Different doses of Dex were intraperitoneally injected before sevoflurane anesthesia; then, the expression of apoptotic-related proteins including BCL-2, BAX and cl-caspase3 as well as amyloid precursor protein (APP, a marker of axonal injury), p-CRMP-2 and CRMP-2 were measured at postnatal days 0, 1and 3 (P0, P1, and P3, respectively). As an antagonist of the bone morphgenetic proteins (BMP) receptor, DMH1 was co-administered with sevoflurane plus Dex to investigate whether BMP/SMAD is associated with the neuroprotective effects of Dex. The results showed that prenatal sevoflurane anesthesia for 4 h activated apoptosis transiently, as manifested by the caspase3 activity peaked on P1 and disappeared on P3. In addition, the expressions of APP and p-CRMP-2/CRMP-2 in postnatal rat hippocampus were significantly increased, which revealed that prenatal sevoflurane anesthesia caused axonal injury of offspring. The long-term learning and memory ability of offspring rats was also impaired after prenatal sevoflurane anesthesia. These damaging effects of sevoflurane could be mitigated by Dex and DMH1 reversed the neuroprotective effect of Dex. Our results indicated that prenatal exposure to 3% sevoflurane for 4 h increased apoptosis and axonal injury, even caused long-term learning and memory dysfunction in the offspring rats. Dex dose-dependently reduced sevoflurane- anesthesia-induced the neurotoxicity by activating the BMP/SMAD signaling pathway.
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