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Post-operative nausea and vomiting (PONV) is a major peri-operative complication. It has numerous adverse consequences that seriously affect the post-operative recovery of patients. The aim of the present study was to investigate the efficacy of intravenous lidocaine in improving PONV and recovery after laparoscopic gynaecological surgery. A total of 40 patients were randomly assigned to 2 groups: Group L (lidocaine group) and Group C (control group). The patients in Group L received intravenous lidocaine throughout the operation, while patients in Group C were given a saline infusion. Vital signs, recovery time, extubation time, dosage of remifentanil, first flatus time and defecation time of each patient were recorded. The incidence of PONV after surgery was also recorded. The recovery of the patients was evaluated by using the quality of recovery score (QoR-40). The total dose of remifentanil was significantly lower in Group L (P<0.05). However, the recovery time and extubation time were shorter in Group C (P<0.05). The first flatus time and defecation time were longer in Group C (P<0.05). The mean arterial pressure and heart rate in Group L were lower and more stable (P<0.05). At 6 h after surgery, the incidence of PONV was significantly lower in Group L vs. that in Group C (P<0.05). The QoR-40 score in Group C was significantly lower at 1 and 3 days after the operation compared with that in Group C (P<0.05). In conclusion, intravenous lidocaine administered to patients undergoing laparoscopic gynaecological surgery may reduce PONV and supports their early recovery [trial registration number in Chinese Clinical Trial Registry: ChiCTR-IOR-17010782 (March 5, 2017)].

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Previous studies have reported the incomplete relaxation effect of neuromuscular blockers on skeletal muscles in acute peritonitis (AP) and other inflammatory processes; however, the underlying mechanisms responsible for this effect have not yet been satisfactorily identified. The impaired removal of cytosolic Ca2+ through sarcoendoplasmic Ca2+-ATPase (SERCA) and defects in sarcoplasmic reticulum (SR) Ca2+ uptake are the major contributing factors to diastolic dysfunction. Previous studies on the effects of neuromuscular blockers have primarily focused on neuromuscular transmission. Because of the reduced calcium uptake in the SR itself, even when neuromuscular transmission is fully blocked, the muscle is not able to relax effectively. In the present study, the impact of AP on rocuronium-induced intraperitoneal pressure reduction and rectus abdominal muscle relaxation, and SERCA uptake function was investigated. AP was induced via gastric perforation and changes in the intraperitoneal pressure before and after the administration of rocuronium were recorded. Muscle contractile properties, uptake and release functions and SERCA activity in the rectus abdominal muscles of AP model rats were measured. The half-relaxation time in the AP group was significantly prolonged compared with that in the control group (P<0.01). The peak rate of SR Ca2+ uptake for whole muscle homogenates was significantly reduced (P<0.05) in AP model rats without reduction of the rate of Ca2+ release evoked through AgNO3. In conclusion, gastric perforation-induced AP attenuates the intraperitoneal pressure-reducing effect of rocuronium, and AP induces diastolic dysfunction of the rectus abdominal muscle. The SR Ca2+-ATPase uptake rate was also reduced by AP.

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INTRODUCTION: The aim of this study was to study the effects of sepsis on diaphragm relaxation properties and the associated expression of sarco-endoplasmic reticulum Ca2+ -ATPase genes SERCA1 and SERCA2. METHODS: Rats were randomized to undergo either sham surgery or cecal ligation and puncture (CLP). Diaphragm isometric relaxation parameters were measured after 24 h. The mRNA expression and protein content of SERCA1 and SERCA2 in diaphragm muscles were determined. RESULTS: Both diaphragm maximal twitch and tetanus relaxation rates were reduced. Twitch half-relaxation time was prolonged after normalization to half of peak twitch tension. The mRNA expression and protein content of SERCA1 and SERCA2 were decreased. CONCLUSIONS: Slowed relaxation of the diaphragm in septic rats was associated with reduced expression of SERCA1 and SERCA2. Muscle Nerve 54: 1108-1113, 2016.

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OBJECTIVE: The explore the mechanism responsible for diaphragmatic contractile and relaxation dysfunction in a rat model of sepsis. METHODS: Thirty-six adult male Sprague-Dawley rats were randomized equally into a sham-operated group and two model groups of sepsis induced by cecal ligation and puncture (CLP) for examination at 6 and 12 h following CLP (CLP-6 h and CLP-12 h groups). The parameters of diaphragm contractile and relaxation were measured, and the calcium uptake and release rates of the diaphragmatic sarcoendoplasmic reticulum (SR) and the protein expressions of SERCA1, SERCA2 and RyR in the diaphragmatic muscles were determined. RESULTS: The half-relaxation time of the diaphragm was extended in both the CLP-6 h and CLP-12 h groups with significantly reduced maximum tension declinerate and the peek uptake rate of SERCA (P<0.01). Diaphragmatic maximum twitch force development rate, the maximal twitch, tetanus tensions and the peek release rate of SR decreased only at 12h after CLP (P<0.01). The expression levels of SERCA1 protein decreased significantly in the diaphragmatic muscles at 12h following CLP (P<0.01) while SERCA2 expression level and SERCA activity showed no significant changes. CONCLUSION: In the acute stage of sepsis, both the contractile and relaxation functions of the diaphragm are impaired. Diaphragmatic relaxation dysfunction may result from reduced calcium uptake in the SR and a decreased level of SERCA1 in the diaphragmatic muscles.

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Hepatocellular carcinoma (HCC) is one of the most malignant types of human primary tumor and has a poor prognosis, therefore, the development of novel therapeutic modalities is necessary. Fatsioside A is a novel baccharane­type triterpenoid glycoside, which is extracted from the fruits of Fatsia japonica. Previous data has revealed that fatsioside A can exert growth inhibition, cell cycle arrest and induce apoptosis in human glioma cells. However, no detailed investigations have been performed to determine its action on human hepatocellular cells, and the exact mechanisms underlying the induction of apoptosis remain to be elucidated. The aim of the present study was to investigate the anticancer effect of fatsioside A in the HepG2 human HCC cell line, and to investigate the underlying mechanisms by focusing on the AMP­activated protein kinase (AMPK) signaling cascade. The results of the present study demonstrated that fatsioside A induced apoptotic death of the human HepG2 HCC cells, which was associated with a marked activation of AMPK and increased expression of the downstream acetyl­CoA carboxylase carboxylase. Inhibition of AMPK by RNA interference or by its inhibitor, compound C, suppressed fatsioside A­induced caspase­3 cleavage and apoptosis in the HepG2 cells, while AICAR, the AMPK activator, elicited marked cytotoxic effects. Together, these results suggested that fatsioside A­induced apoptotic death requires AMPK activation in HepG2 cells.

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BACKGROUND: Etomidate may affect adrenocortical function. We conducted an investigation of the comparative effects of etomidate and propofol during electroconvulsive therapy (ECT) on adrenocortical function and hemodynamics. METHODS: Patients in group T received etomidate and those in group B received propofol during intravenous anesthesia in ECT. Patients underwent ECT once every 2 days for 6 times. The serum levels of cortisol (Cor) and adrenocorticotropic hormone were determined 5 minutes before first anesthesia (baseline level, D0), and 24 hours (D1) as well as 48 hours after the last ECT (D2). At the same time, the hemodynamics was measured 2 minutes before anesthetic induction (T0), 30 seconds (T1) and 20 minutes after ECT (T2). Electrographic seizure duration (t), average seizure energy index, and postictal suppression index were recorded. RESULTS: Compared with the baseline level, serum Cor levels in group T were markedly decreased, but in normal ranges, at 24 hours after second and sixth treatments. No significant difference in serum Cor level was observed between the baseline and 48 hours posttreatment. In group B, there was no significant difference in serum Cor level between the baseline and 24 hours as well as 48 hours after each treatment. Furthermore, no significant difference in adrenocorticotropic hormone level was observed between the baseline and 24 hours as well as 48 hours posttreatment. However, the hemodynamics markedly changed during ECT and reached the preanesthetic level at 20 minutes posttreatment. The ECT-induced seizure duration in group T was longer than that in group B. However, seizure energy index and postictal suppression index was not significantly different between groups T and B. CONCLUSIONS: Etomidate and propofol would not affect the adrenocortical function during ECT, and hemodynamics reached normal level in a short time after ECT. Etomidate and propofol were both safe intravenous anesthetics during ECT, although etomidate was associated with comparatively longer seizure duration.

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Shellfish samples were prepared by microwave, and 27 microelements including Ca, Mg, K, Na, P, S, Zn, Mn, Fe, Cu, Cr, Co, Se, Sn, Ni, Al, Ti, V, Mo, Ba, Ge, Si, Cd, I, Pb, As and Hg were determined by ICP-AES. It was showed that ICP-AES had an obvious advantage in the determination of microelements, and shellfishes contained upwards of 20 kinds of microelements. Calcium in fresh water was higher than that in seawater, and As and Pb were the major pollutants.

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