Objective To explore the influence of gentamycin on murine cochlea spiral ganglion neurons' electrophysiological properties and its significance.Methods Using whole-cell voltage clamp technique, we studied gentamycin's influence on the peak currents of the potassium and sodium ion channels on cell membranes of acutely dissociated murine spiral ganglion neurons,the relationship to gentamycin's concentration in extracellular fluid, and the currents' recovery after gentamycin being washed out.Results Gentamycin could inhibit voltage-dependent potassium channels, but it couldn't inhibit voltage-dependent sodium channels. Gentamycin's inhibitation on potassium currents had dose-dependence with gentamycin's concerntration in extracellular fluid and the currents recoverd incompletely after gentamycin being washed out.Conclusion This research explained the ototoxic mechanism of gentamycin through its action on keeping from spiral ganglion neurons' potassium ion channels from the electrophysiological aspect, and set a foundation for further research.

Objective To investigate the effects of remifentanil on large-conductance Ca2+ -activated potassium channel (BKCa) in human mesenteric arterial smooth muscle cells (MASMCs) and the mechanism of the vasorelaxant effect of remifentanil. Methods Human MASMCs were obtained freshly by the method of enzymolysis. BKCa current (IBKCa) was recorded by the whole-cell patch clamp technique. The changes in IBKC. produced by different concentrations of remifentanil (1.2, 4.8, 19.4, 77.4 and 310.0 nmol/L) with the holding potential of + 80 mV were observed. BKCa activation rate was calculated. Results Remifentanil significantly increased IBKCa,moved Ⅰ-Ⅴ curve upward and had no effect on the threshold of activation for IBKCa . With the increase in the concentration of remifentanil, BKCa activation rate increased gradually (P ＜ 0.01), and it remained stable when the concentration reached 19.4 nmol/L. There was no significant difference in the peak time of IBKCa after different concentrations of remifentanil were given (P ＞ 0.05). Logarithmic curve was found to suit the relationship between the concentration of remifentanil and BKCa activation rate and the IC50 concentration was (118 ± 7) nmol/L. Conclusion Remifentanil results in vasorelaxation by activating BKCa in MASMCs in a concentration-dependent manner.

Objective To observe the efficacy and safety in the postoperative craniocerebral trauma elderly patients us-ing the layered method of sputum suction. Methods Senventy patients aged 60 and above with craniocerebral trauma were divided into the layered method group (group A) and the traditional method group (group B). The vital sign, mu-cosa damage frequency, the times of average daily sputum suction and the incidence of VAP were compared. Results Compared with group B, group A could reduce the vital signs change and the times of average daily sputum suction, with lower airway mucosa damage and the incidence of VAP, the difference was statistically significant(P<0.05). Con-clusion The layered method of sputum suction is safer and more effective than traditional method in treatment of the postoperative elderly patients with craniocerebral trauma.

Objective:To observe the effect of systematic graded rewarming measures on body temperature and prognosis of patients with moderate and severe trauma [revised trauma score (RTS) < 12] requiring emergency operation.Methods:A prospective randomized double-blind controlled study was conducted. From January 2020 to January 2021, 104 patients who underwent emergency trauma surgery in the Second Affiliated Hospital of Wenzhou Medical University were selected as the research object. According to random number table method, the patients were divided into traditional rewarming group and systematic graded rewarming group, with 52 cases in each group. Patients in traditional rewarming group (only record the body temperature without intervention, and start the rewarming process when the body temperature at any time was less than 36 ℃); the patients in the system graded rewarming group start the preventive measures as soon as they were admitted to the hospital, and record the body temperature. When the body temperature at any time was less than 36 ℃, start the graded rewarming process. Observe the rewarming effect, coagulation function, blood gas analysis and postoperative anesthesia recovery time of the two groups and final outcome.Results:With the extension of time, the body temperature of the two groups increased gradually. The body temperature of the systematic grade rewarming group was significantly higher than that of the traditional rewarming group at 2 hours after rewarming and at discharge (℃: 36.23±0.77 vs. 35.84±0.93 at 2 hours after rewarming, 36.54±0.87 vs. 35.82±0.92 at discharge, both P < 0.05). The incidence of subsequent hypothermia was significantly lower than that in the traditional rewarming group [7.7% (4/52) vs. 25.0% (13/52), P < 0.05]. The postoperative activated partial thromboplastin time (APTT) of the two groups was significantly shorter than that at admission (s: 35.74±8.05 vs. 45.55±28.02 in the systematic rewarming group, P < 0.05; 38.35±6.48 vs. 42.40±13.18 in the traditional rewarming group, P < 0.05); the intraoperative and postoperative pH values in the systematic rewarming group were significantly higher than those at admission (7.33±0.05, 7.36±0.06 vs. 7.30±0.07, both P < 0.05), while there was no significant difference between the intraoperative and postoperative pH values in the traditional rewarming group and those at admission (7.31±0.06, 7.33±0.06 vs. 7.31±0.05, both P > 0.05). The postoperative prothrombin time (PT) and anesthesia recovery time in the systematic graded rewarming group were significantly shorter than those in the traditional rewarming group [PT (s): 15.05±2.44 vs. 17.94±3.48, anesthesia recovery time (hours): 14.40±11.76 vs. 17.35±10.51, all P < 0.05], and the pH value was significantly higher than that in the traditional rewarming group (7.36±0.06 vs. 7.33±0.06, P < 0.05). The systematic graded rewarming group had higher improvement rate and lower disability rate than the traditional rewarming group (76.9% vs. 65.4% and 17.3% vs. 25.0%, both P < 0.05). Conclusion:Systematic graded rewarming measures can improve the hypothermia of emergency trauma patients who received surgery, reduce the incidence of subsequent hypothermia of trauma patients, shorten the time of postoperative resuscitation, improve the coagulation function and blood gas indexes, improve the treatment rate, and reduce the incidence of disability.

Inflammatory orofacial pain, in which substance P (SP) plays an important role, is closely related to the cross-talk between trigeminal ganglion (TG) neurons and satellite glial cells (SGCs). SGC activation is emerging as the key mechanism underlying inflammatory pain through different signalling mechanisms, including glial fibrillary acidic protein (GFAP) activation, phosphorylation of mitogen-activated protein kinase (MAPK) signalling pathways, and cytokine upregulation. However, in the TG, the mechanism underlying SP-mediated orofacial pain generated by SGCs is largely unknown. In this study, we investigated whether SP is involved in inflammatory orofacial pain by upregulating interleukin (IL)-1β and tumour necrosis factor (TNF)-α from SGCs, and we explored whether MAPK signalling pathways mediate the pain process. In the present study, complete Freund's adjuvant (CFA) was injected into the whisker pad of rats to induce an inflammatory model in vivo. SP was administered to SGC cultures in vitro to confirm the effect of SP. Facial expression analysis showed that pre-injection of L703,606 (an NK-1 receptor antagonist), U0126 (an inhibitor of MAPK/extracellular signal-regulated kinase [ERK] kinase [MEK] 1/2), and SB203580 (an inhibitor of P38) into the TG to induce targeted prevention of the activation of the NK-1 receptor and the phosphorylation of MAPKs significantly suppressed CFA-induced inflammatory allodynia. In addition, SP promoted SGC activation, which was proven by increased GFAP, p-MAPKs, IL-1β and TNF-α in SGCs under inflammatory conditions. Moreover, the increase in IL-1β and TNF-α was suppressed by L703, 606, U0126 and SB203580 in vivo and in vitro. These present findings suggested that SP, released from TG neurons, activated SGCs through the ERK1/2 and P38 pathways and promoted the production of IL-1β and TNF-α from SGCs, contributing to inflammatory orofacial pain associated with peripheral sensitization.