Effect of remifentanil combined with sevoflurane inhalation anesthesia on coagulation function and postoperative recovery of patients undergoing endoscopic selective varices devascularization.

OBJECTIVE: To investigate the effect of remifentanil combined with sevoflurane inhalation anesthesia on coagulation function and postoperative recovery of patients undergoing endoscopic selective varices devascularization (ESVD). METHODS: Altogether 116 patients undergoing ESVD in our hospital were randomly divided into two groups. The control group received propofol combined with remifentanil anesthesia, while the observation group received remifentanil combined with sevoflurane inhalation anesthesia. RESULTS: There was no statistical difference in coagulation function indexes between the control group and the observation group (P>0.05), and the clinical anesthesia effect of the observation group was better (P<0.001). Five minutes after intubation, compared with the control group, the clinical stress response index was better (all P<0.001), the quality of anesthesia recovery was higher (all P<0.001), the heart rate was better after anesthesia (P<0.001), and the incidence of adverse reactions was higher (P<0.01) in the observation group. CONCLUSION: Compared with remifentanil combined with propofol anesthesia, remifentanil combined with sevoflurane inhalation anesthesia for ESVD can effectively improve the clinical anesthesia effect, improve the quality of anesthesia recovery, and reduce stress reactions, but the incidence of adverse reactions is increased. Therefore the clinical application still needs to be strengthened.

Annexin A2-modulated proliferation of pulmonary arterial smooth muscle cells depends on caveolae and caveolin-1 in hepatopulmonary syndrome.

We have established that annexin A2 (ANXA2) is an important factor in the experimental hepatopulmonary syndrome (HPS) serum-induced proliferation of pulmonary arterial smooth muscle cells (PASMCs). However, the detailed mechanism remains unclear. ANXA2 translocated to the caveolin-enriched microdomains (caveolae) in PASMCs upon HPS serum stimulation. The disruption of caveolae by Methyl-ß-cyclodextrin (MßCD) alleviated the caveolae recruitment of ANXA2 and the ANXA2-mediated activation of ERK1/2 and NF-κB, so that ANXA2-modulated PASMC proliferation was suppressed. The over-expression of Cav-1 resulted in the relocation of ANXA2 from caveolae and negatively regulated ERK1/2 and NF-κB activation, which inhibited the ANXA2-modulated PASMC proliferative behavior. These data indicate that caveolae function as a signaling platform for ANXA2-induced proliferative behavior and Cav-1 participates upstream of ANXA2 in the activation of ERK1/2 and NF-κB.