Objective To establish an HPLC method for the determination of artesunate in artesunate and amodiaquine hydrochloride tablets. Methods WondaSil C18-WR column was used with mobile phase consisted of acetonitrile:phosphoric acid aqueous solution(adjust pH to 3,gradient elution);wavelength was 210 nm; flow rate was 1 mL/min and the column temperature was 30℃.Results The standard curve was linear in the range of 0.2~3.2 mg/mL(r=0.9997), average recoveries were 99.0%(RSD=1.35%, n=6).Conclusion The method is accurate and sensitive, and it can be used to control the quality of artesunate and amodiaquine hydrochloride tablets.

Objective To investigate the effect of propofol on apoptosis at different time points after focal cerebral ischemia-reperfusion (I/R) in a rat model of reversible middle cerebral artery occlusion (MCAO). Methods Sixty male SD rats weighing 240-260g were randomly divided into 2 groups ( n = 30 each): propofol group received intraperitoneal (i. p.) propofol 80 mg ?kg before MCAO and control group received equal volume of normal saline instead of propofol. The animals were anesthetized with 10% chloral hydrate 350mg?kg-1 i.p. . The right external, internal and common carotid artery were exposed. A 4-0 nylon thread with rounded tip was inserted via external carotid artery into internal carotid artery and threaded cranially until resistance was felt. MCAO was maintained for 90 min before reperfusion. The animals were killed and brains removed for detection of apoptotic neurons using TUNEL staining combined with electronic microscopic examination at 3 h, 6 h, 24 h, 3 days, 5 days and 7 days after reperfusion was started ( n = 5 at each time point in both groups) . Results In control group the ratio of apoptotic neurons peaked at 24 h of reperfusion and then gradually decreased; while the ratio of TUNEL positive neurons kept on increasing indicating a shift from apoptosis to necrosis after 24 h reperfusion. The ratio of TUNEL positive neurons and apoptosis were significantly lower in propofol group than in control between 6 h to 3 days after reperfusion was started. Conclusion Propofol pretreatment attenuates apoptosis induced by focal cerebral I/R and the maximum effect is reached and maintained between 6 h to 3 days of reperfusion.

120 g?L-1. The estimated intraoperative blood loss was 1 000-1 500 ml. The patients were randomly divided into 3 groups ( n = 16 each): group Ⅰ lactated Ringer's solution (LR); group Ⅱ LR-6% HES and group Ⅲ colloid (6% HES). Blood was removed from radial artery after induction of anesthesia. The target Hct was 28% . The volume of blood removed = body weight (kg)?7.5 ? (preop Hct -target Hct) / 0.5?(preop Hct + target Hct). The removed whole blood was replaced with lactated Ringer's solution in a three to one ratio in group Ⅰ or with 6% HES in a one to one ratio in group Ⅲ. In group Ⅱ half of the removed whole blood was replaced with LR and the other half with 6% HES. The EVLW, HR, BP, Cardiac index (CI) and dp/dtmax were monitored by PiCCO and recorded before induction of anesthesia (T0), immediately after induction of anesthesia (T1), immediately after and 15 min after ANH (T2,3), immediately before and after reinfusion (T4,5) . Hct, colloid osmotic pressure and blood gases were also measured and recorded. Results The 3 groups were comparable with respect to M/F ratio, age, body weight and the volume of whole blood removed. MAP, HR, SpO2 and CVP were stable during operation in all 3 groups. Hct was significantly decreased after ANH as compared with the baseline at T0 in all 3 groups. The osmotic pressure was significantly decreased after ANH in group Ⅰ and Ⅱ and was significantly higher in group Ⅱ and Ⅲ than in group Ⅰ after ANH. CI and dp/dtmax were significantly decreased after ANH as compared to the baseline at T0 in all 3 groups. There was no significant difference in EVLW, PaO2 and [ HCO3- ] among the 3 groups. Conclusion Moderate ANH with crystalloid or colloid has little effect on EVLW and oxygenation in patients with normal cardio-pulmonary function.

Objective To research the different protective effects of general anesthesia combined with thoracic epidural anesthesia on experimental myocardial infarctionMethods Rabbits of experimental group were anesthesitized with 1% sodium pentobarbitone (30 mg/kg, iv) Following tracheal intubation, epidural catheter was put into at T_ 6-7 with the anterior end of the catheter reaching at T_ 2-3 After the epidural anesthesia was made sure to be effective, the anterior descending branches of left coronary artery were ligated Blood samples were collected before ligation, 15, 30, 60, 120, 180 and 240 min after ligation All procedures of control group were similar to those of experimental group except for thoracic epidural anesthesia Nitric oxide (NO), creatine kinase(CK), lactate dehydrogenase (LDH), aspartate transaminase (AST), superoxide dismutase (SOD) were detected The changes of the activities of CK and LDH, and NO level during the research course in both groups were analyzed with liner regression Results The regression coefficients of CK, LDH and NO in the experimental group were significantly lower than those in control group In the experimental group the activities of CK and LDH decreased markedly, NO level increased significantly as compared with those in control groupConclusions General anesthesia combined with thoracic epidural anesthesia produces the protective effects on the myocardial infarction and the stress-induced injury

Objective To research the stress to experimental myocardial infarction under general anesthesia combined with thoracic epidural anesthesia(TEA) Methods Nine rabbits in experimental group were anesthetized with 1% sodium pentobarbitone with tracheal intubation after sectioned, and after the epidural catheters was put into to make sure that the epidural anesthesia was effective, the anterior descending branches of their left coronary artery were ligated All procedures in control group were similar to those of experimental group except for thoracic epidural anesthesia The blood samples from left common carotid artery before ligation were taken 15,30,60,120,180 and 240min after ligation, to measure the plasma levels of monoamine neurotransmitters with high performence liquid chromatography, the Ag Ⅱ and cortisol levels with radioimmunoassay TNFa content in non infarction myocardium was assessed with immunohistochemistry Results There were no differences in NE and 5 HT levels between both groups before ligation Thirty min after the ligation, NE level in experimental group remained unchanged, but in control group increased markedly(P

Objective To evaluate the effect of thoracic epidural block combined with general anesthesia on c-fos and heat shock protein(HEP) 70 gene expression of myocardium from non-infarct area in rabbits with acute myocardial infarction. Methods Twenty-eight New Zealand white rabbits of either sex (12 male, 16 female), weighing 2.5-3. 8kg were randomly divided into two groups with 14 animals in each group: general anesthesia group and combined general-epidural anesthesia group. The rabbits were anesthetized with 1 % pentobarbital and tracheotomized and intubated. Spontaneous breathing was maintained. Epidural catheter was placed with one of the tips reaching T2-3. 2% lidocaine was injected and the effectiveness of epidural block was confirmed by decrease in MAP. Left common carotid artery was cannulated for intra-arterial pressure monitoring. Chest was then opened, and anterior descending branch of left coronary artery was ligated. Myocardial infarction was confirmed by changes in ECG. 4 hours after ligation the animals were sacrificed and a piece of myocardium from non-infarct area was taken for measurement of the concentration, OD and ratio of total RNA in 100 mg of myocardium. 0.7 ?g of total RNA was used for determination of c-fos and HPS 70 expression relative to ?-actin gene(c-fos/ ?-actin, HSP70/ ?-actin) by using one-step RT-PCR. Results c-fos/ ?-actin and HSP70/ ?-actin were significantly lower in combined general-epidural anesthesia group than those in control group(P

Acute Disease ; Adult ; Humans ; Male ; Occupational Diseases ; diagnosis ; therapy ; Phosphines ; poisoning ; Poisoning ; diagnosis ; therapy

Objective: To investigate the ultrastructural pathogenesis of retina injury by observing the ultrastructural changes under the transmission electron microscope(TEM) after ocular blast injury in rabbits.Methods: Ocular blast injury models were set up in 20 rabbits by the bow wave produced with a bioshock tube.The rabbits were sacrificed at scheduled times after injury,their retinas obtained and their ultrastructural changes observed by TEM.Results: The axonal ultrastructural changes of the retina induced by blast were summarized as follows.The microfilaments and microtubules were swollen and distorted in the early stage,followed by reactive swelling of the ganglion cells.The swollen mitochondria and endoplasmic reticula focally accumulated and the cytoskeleton was destroyed.Finally the intraaxonal cellular structure disappeared and the axon disconnected.Conclusion: Ocular blast injury may cause retinal ultrastructural changes.The pathological changes of ganglion cells in the optic nerve may be associated with the direct effect of the blast and/or ischemia and are possibly important factors in the pathogenesis of vision disturbance.

The G protein-coupled estrogen receptor (GPER), also known as G protein-coupled receptor 30 (GPR30), was identified in the recent years as a functional membrane receptor different from the classical nuclear estrogen receptors. This receptor is widely expressed in the cortex, cerebellum, hippocampus, heart, lung, liver, skeletal muscle, and the urogenital system. It is responsible for the mediation of nongenomic effects associated with estrogen and its derivatives, participating in the physiological activities of the body. The present study reviews the molecular structure, subcellular localization, signaling pathways, distribution, and function of GPER in the male reproductive system.
Estrogens ; metabolism ; Genitalia, Male ; metabolism ; Humans ; Male ; Molecular Structure ; Organ Specificity ; Receptors, Estrogen ; chemistry ; physiology ; Receptors, G-Protein-Coupled ; chemistry ; physiology ; Reproduction ; physiology ; Signal Transduction

OBJECTIVETo investigate the expressions of sphingosine-1-phosphate receptors 1-3 (S1P1- 3) in the corpus cavernosum of castrated male rats and its relationship with the NOS/NO/cGMP and RhoA/Rho kinase signaling pathways.

METHODSWe equally randomized 18 eight-week-old healthy male SD rats into a sham-operation control, a castration, and a testosterone replacement (TR) group and harvested the bilateral testes and epididymides from the rats in the latter two groups, followed by 4 weeks of subcutaneous injection of testosterone propionate at 3 mg per kilogram of the body weight per day for those in the TR group and that of plant oil for those in the control and castration groups. At the age of 12 weeks, we measured the serum testosterone (T) level and maximum intracavernous pressure/mean arterial pressure (ICPmax/MAP) of the animals and determined the expressions of SlP1-3, eNOS, P-eNOS, ROCK1, and ROCK2 in the corpus cavernosum by Western blot and immunohistochemistry.

RESULTSThe serum T level was significantly decreased in the rats of the castration group as compared with those of the control and TR groups ([0.41 ± 0.04] vs [16.01 ± 1.02] and [15.84 ± 1.32] nmol/L, P < 0.01), with no statistically significant difference between the latter two groups. The ICPmax/MAP at 0 V, 3 V, and 5 V electric stimulation was remarkably lower in the rats of the castration group (0.088 ± 0.014, 0.323 ± 0.014, and 0.432 ± 0.012) than in those of the control group (0.155 ± 0.011, 0.711 ± 0. 010, and 0.819 ± 0.024) and TR group (0.153 ± 0.012, 0.696 ± 0.017, and 0.763 ± 0.027) (P < 0.01), with no significant difference between the latter two groups. With GAPDH as internal control, the animals of the castration group showed markedly reduced expressions of S1P1 ([49.99 ± 3.39]%), eNOS ([46.82 ± 3.81]%) , and P-eNOS ([45.42 ± 4.35]%) in comparison with those in the control group ([72.57 ± 3.06], [89.76 ± 3.98], and [82.53 ± 8.92] and TR group ([71.77 ± 4.43], [87.19 ± 4.23], and [79.82 ± 7.38]%) (P < 0.01) , while the expressions of S1P2, S1P3, ROCK1, and ROCK2 were significantly upregulated in the castration group ([82.35 ± 4.13], [61.03 ± 5.14], [74.50 ± 4.02], and [69.83 ± 5.75]%) as compared with those in the control group ([41.67 ± 1.68], [31.66 ± 2.67], [35.69 ± 5.56], and [39.85 ± 7.17]%) and TR group ([42.80 ± 3.87], [32.25 ± 4.22], 38.06 ± 5.21], and [42.36 ± 4.44]%) (P < 0.01).

CONCLUSIONAndrogen deficiency induces significant reduction of ICPmax/ MAP in male rats, which is possibly associated with the decline of S1P1 in the corpus cavernosum, inhibition of the eNOS/NO/cGMP signaling pathway, increased expressions of S1P2 and S1P3, and activation of the RhoA/Rho kinase signaling pathway.

Animals ; Male ; Nitric Oxide Synthase Type III ; metabolism ; Orchiectomy ; Penis ; metabolism ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Receptors, Lysosphingolipid ; metabolism ; Testosterone ; blood ; pharmacology ; rho-Associated Kinases ; metabolism