By using the whole-cell clamp-patch technique, the effects of dexamethasone on calcium channel current (Ica) and nicotine receptor channel current (I_(NIC)) were examined. The acute action of glucocorticoid on adrenal medullary chromaffin cell (AMCC) of rats was a significant inhibition of I_(NIC), while no apparent effect was observed on Ica induced by electricity. The results suggest that the acute action of glucocorticoid on catecholamine release in rat AMCC may be directly related to nicotine receptor.

Objective To observe the influence of Zhenweifang on the muscle tension in flaccid paralysis period and prognosis of stroke.Methods One hundred and eighty patients were randomly divided into basic group,Buyanghuanwutang group and Zhenweifang group.Basic group was treated with usual medical treatment with nerve rehabitilation and acupuncture.Buyanghuanwutang group and Zhenweifang group were given the corresponding traditional Chinese medicine.Patients in Buyanghuanwutang group and Zhenweifang group stop taking the traditional Chinese medicine when their muscle tension reach the level of Ashworth Grade Ⅱ,and continued their basic treatment.The defect of neurological and daily life ability were evaluated after three-week and six-week treatment,and the prognosis was evaluated according to clinical efficacy.Results The time that patients muscle tension in Zhenweifang group need to reach Ashworth Grade Ⅱ was much shorter than that in Buyanghuanwutang group and basic group(P

AIM: To study the effects of calcium channel blockers (CCB) on nicotinic acetylcholine receptor current (I_(NIC)) in rat adrenal medullar chromaffin cells (RAMCs). METHODS: By using the whole-cell clamp-patch technique, we have investigated the effects of nifedipine(NIF)、?-conotoxin GVIA and ?-agatoxin IVA on I_(NIC) induced by nicotine(NIC) before and after RAMCs perfusion. RESULTS: After perfusing RAMCs for 5 min, different kinds of calcium channel blockers at different concentration showed significant inhibitory effects on I_(NIC) induced by 50 ?mol/L NIC. The peak inhibition rates of 10 ?mol/L NIF、400 nmol/L ?-conotoxin GVIA and 100 nmol/L ?-agatoxin IVA were (61.7?5.1)%,(29.3?7.4)% and (17.6?7.5)%, respectively. CONCLUSION: The acute effects of different kinds of CCBs on RAMC were that they obviously inhibited I_(NIC) induced by NIC. These results suggest that CCBs may inhibit catecholamine secretion by directly blocking nicotinic acetylcholine receptor channel. [

As a social problem,college students'Internet Addiction has drawn attention widely.A lot of domestic areas and departments have done research on college students' Internet Addiction and achieved some sucess.On the basis of retrieval of papers on students' Internet Addiction,this article analyzes former research and brought up some proposals for the future research aimed at its deficiences.

Objective:To analyze the feature of anaphylactic shock induced by alprostadil injection. Methods: Totally 1624 pa-tients treated with alprostadil injection in our hospital from January to March 2014 were undergone adverse drug reaction monitoring. Six cases of anaphylactic shock induced by alprostadil injection were statistically analyzed. Results:6 cases of anaphylactic shock induced by alprostadil injection occurred in the department of intervention and most of thd reaction happened in arterial injection. Two lot num-ber of drugs were in high frequency. Patients showed a sharp fall in blood pressure, chest discomfor, palpitation, shortness of breath, paleness, sweating and other symptoms. After anti allergy, blood pressure, oxygen the rapy and other treatment measures vital signs gradully stabilized. Conclusion:Anaphylactic shock induced by alprostadil injection is in correlation with the administration mode of artery injection. The change of the patient' s condition and vital signs should be closely observed when we inject the patient with alpros-tadil injection. We must prevent the occurrence of serious adverse reactions.

To investigate the role of ligustrazine on relaxation of the isolated rabbit corpus cavernosum tissue in vitro, the effects of ligustrazine on the corpus cavernosum were observed by using experimental method of smooth muscle strips. Concentration-responses to phenylephine (PE) and KCl were recorded. The results showed that ligustrazine concentration-dependently depressed the contraction response of smooth muscle strips induced by PE. The maximum percentage relaxation of cavernosal strips by ligustrazine was 74.1% +/- 6.2% (compared with control: 21.9% +/- 5.6%, P < 0.01). Ligustrazine concentration-dependently reduced the amplitude of the contraction induced by cumulative doses of PE or KCl, shifted the cumulative concentration response curves of PE and KCI to the right and depressed their maximal responses. It was concluded that ligustrazine could significantly relax the cavernosal muscle contraction induced by PE in vitro. The results suggested that ligustrazine inhibited calcium ion influx.
Calcium Channels/drug effects ; Muscle Contraction/*drug effects ; Muscle Relaxation/*drug effects ; Muscle, Smooth/*drug effects ; Muscle, Smooth/physiology ; Penis/*drug effects ; Penis/physiology ; Phenylephrine/pharmacology ; Potassium Chloride/pharmacology ; Pyrazines/*pharmacology

Objective:To evaluate the effect of sevoflurane on necroptosis in isolated hippocampal neurons and the relationship with ryanodine receptor.Methods:Primarily cultured hippocampal neurons of fetal rats of Sprague-Dawley rats were inoculated in culture wells (100 μl/well) or culture flasks (3 ml/bottle) at a density of 5×10 5 cells/ml at 7 days of culture and divided into 3 groups ( n=24 each) using a random number table method: control group (group C), sevoflurane group (group S) and ryanodine receptor antagonist group (group R). Group C received routine culture.Ryanodine receptor antagonist Dantrolene at a final concentration of 3 μmol/L was added in group R. Thirty minutes later, the cells were placed in the incubator containing 2% sevoflurane and cultured for 5 h at 37 ℃ in S and R groups.Then cells were collected, the morphology of neurons was observed with an inverted microscope, the concentrations of free calcium ion ([Ca 2+ ] i) in cytoplasm were determined by flow cytometry, the expression of ryanodine receptor and phosphorylated MLKL protein (p-MLKL) was detected by Western blot, the expression of RIP3 was measured by immunofluorescence, and necroptosis rate was calculated. Results:Compared with group C, the [Ca 2+ ] i were significantly increased, the expression of ryanodine receptor and p-MLKL was up-regulated, and the necroptosis rate was increased in S and R groups ( P<0.05). Compared with group S, the expression of ryanodine receptor and p-MLKL was significantly down-regulated, and the [Ca 2+ ] i and necroptosis rate were decreased in group R ( P<0.05). There was no obvious abnormality in the morphology of neurons in group C. The cell body of neurons were shrunk, the processes were broken, and the network between processes was sparse in group S. The cell body was round, and the morphology was close to normal in group R. Conclusion:Sevoflurane can cause necroptosis in isolated hippocampal neurons of rats, and the mechanism is related to up-regulating the expression of ryanodine receptors and leading to calcium overload.

Objective To evaluate the effect of nimodipine on the activity of calcineurin (CaN) in the hippocampus of aged rats.Methods Sixty healthy male Sprague-Dawley rats,aged 18 months,weighing 550-650 g,were divided into 2 groups (n=30 each) using a random number table:surgery group (group S) and nimodipine group (group N).Nimodipine 1 mg/kg was intraperitoneally injected in group N,while the cqual volume of normal saline was given instead in group S,and 30 min later exploratory laparotomy was performed.Ten rats in each group were randomly selected on 1 day before operation and 3 and 7 days after operation,and Morris water maze test was performed.After the end of Morris water maze test,10 rats were selected and sacrificed,brains were removed,and hippocampi were isolated for detection of apoptosis in hippocampal neurons (by flow cytometry) and expression of CaN,phosphor-BAD (p-BAD) and caspase-3 in hippocampal tissues (by Western blot).Apoptotic rate was calculated.Results Compared with the value at 1 day before operation,the escape latency was significantly prolonged,the frequency of crossing the original platform was decreased,the time of staying at the platform quadrant was shortcned,apoptotic rate was increased,and the expression of CaN,p-BAD and caspase-3 in hippocampal tissues was up-regulated at each time point after operation in group S (P＜0.05).Compared with group S,the escape latency was significantly shortened,the frequency of crossing the original platform was increased,the time of staying at the platform quadrant was prolonged,apoptotic rate was decreased,and the expression of CaN,p-BAD and caspase-3 in hippocampal tissues was down-regulated at each time point after operation in group N (P＜0.05).Conclusion The mechanism by which nimodipine inhibits apoptosis in hippocampal neurons and reduces postoperative cognitive dysfunction may be related to inhibition of CaN activation in aged rats.

Objective To evaluate the effect of nimodipine combined with 7.5％ hypertonic saline (HS) on postoperative cognitive function in aged rats.Methods Ninety-six healthy male Wistar rats,aged 18 months,weighing 450-500 g,were assigned into 4 groups (n=24 each) using a random number table:splenectomy group (group S),nimodipine group (group N),group HS and nimodipine plus HS group (group N+HS).Nimodipine 1 mg/kg was intraperitoneally injected in group N.In group HS,7.5％ HS 4 ml/kg was injected via the caudal vein.The equal volume of normal saline was injected intraperitoneally or via the caudal vein in group S.Splenectomy was performed under sevoflurane anesthesia at 30 min after the end of administration.On 1 day before operation and 3 and 7 days after operation,Morris water maze test was performed,and blood sainples from the caudal vein were simultaneously collected for determination of the concentrations of serum S100β protein and neuron-specific enolase (NSE) by enzyme-linked immunosorbent assay.Results Compared with group S,the frequency of crossing the original platform was significantly increased,the escape latency was shortened,and the concentrations of serum S100β protein and NSE were decreased at each time point after operation in N,HS and N+HS groups (P＜0.05).Compared with group N or group HS,the frequency of crossing the original platform was significantly increased,the escape latency was shortened,and the concentrations of serum S100β protein and NSE were decreased at each time point after operation in group N+HS (P＜0.05).Conclusion Nimodipine combined with 7.5％ HS exerts better efficacy than either alone in improving postoperative cognitive function in aged rats.