The effect of lidocaine on hemodynamics in self-retaining laryngoscope / 中国基层医药

ObjectiveTo observe the different mode of administration of lidocaine on hemodynamic effects during self-retaining laryngoscope.Methods75 adult patients,underwent selective operations of removal and biopsy of the vocal polype,epiglottis or laryngeal tumor via self-retaining laryngoscope under general anesthesia,were randomly divided into three groups,with 25 cases for each.Group Ⅰ was the control group; Group Ⅱ was the throat spraying group;Group Ⅲ was the intravenous drug group.The incidence of irritating cough and the changes of mean arterial pressure(MAP) and hear rate(HR) were observed during operations.ResultsThe incidence of irritating cough in group Ⅱ was lower than in group Ⅰ and group Ⅲ ( all P ＜ 0.05 ).MAP,HR in group Ⅱ was also lower than that in group Ⅰ and Ⅲ during extubation( all P ＜0.05).However there were no significant differences on MAP,HR between group Ⅰ and group Ⅲ during extubation( all P ＞ 0.05 ).ConclusionLidocaine spraying on larynx could alleviate irritating cough and had significant preventive effect on cardiovascular response,and the effect in this method was superior to intravenous injection.

Fluvastatin, a lipophilic statin, induces apoptosis in human hepatocellular carcinoma cells through mitochondria-operated pathway.

Fluvastatin, a lipophilic statin, was known to inhibit proliferation and induce apoptosis in many cancer cells. Its potential anticancer was evaluated in three hepatocellular carcinoma (HCC) cell lines (HepG2, SMMC-7721 and MHCC-97H). Cells were treated with fluvastatin in vitro and its effect on cell proliferation, cell cycle, invasion and apoptosis was determined. Mechanism of apoptosis induced by fluvastatin on HCC cell lines was also investigated through western blotting and mitochondrial membrane potential (MMP) analysis. It was observed that fluvastatin inhibited proliferation of HCC cells by inducing apoptosis and G2/M phase arrest in a dose-dependent manner. The results of cell invasion assay revealed that fluvastatin significantly decreased the invasion potency of HCC cells. A mitochondria-operated mechanism for fluvastatin induced apoptosis might be involved and was supported by Western blotting and MMP analysis. After fluvastatin treatment, expression of Bcl-2 and procaspase-9 were downregulated, cytochrome c (cytosolic extract), Bax and cleaved-caspase-3 protein expression were increased. Furthermore, a breakdown of MMP in HCC cells was observed. To conclude, these results have provided a rationale for clinical investigations of fluvastatin in future as a potential anticancer reagent for growth control of HCC.