Objective To investigate the effect of valsartan combined with amlodipine in treatment of elderly patients with essential hypertension and diabetes,and to provide a reference for the development of clinical treatment. Methods 339 patients with essential hypertension complicated with diabetes in our hospital were randomly divided into 3 groups:A group,B group and C group,each group in 113 cases.A group was treated with amlodipine tablets,B group was treated with valsartan capsules,and C group was treated with amlodipine tablets combined with valsartan capsules.After 3 months of continuous treatment,blood pressure,blood glucose,blood lipids and uric acid were com-pared among the three groups before and after treatment.Results The three groups of patients before treatment, systolic blood pressure and diastolic blood pressure had no significant difference;The three groups of patients after treatment,systolic blood pressure and diastolic blood pressure were significantly lower than before treatment;After treatment in C group,the systolic blood pressure was (135.70 ±8.17)mmHg,which was significantly lower than (139.42 ±8.29)mmHg in A group and (139.52 ±7.48)mmHg in B group,the difference was statistically significant (t =3.77,3.81,all P <0.05);The three groups of patients after treatment of diastolic blood pressure had no significant difference,and there were no statistical significance among the three groups before treatment in the fasting blood glucose,fasting insulin,ISI level difference;Of A group after treatment,the fasting blood glucose,fasting insulin,ISI levels were (7.63 ±0.89)mmol/L,(16.11 ±2.39)mIU,(-4.26 ±0.35),there were no significant difference before and after treatment;Of B group and C group after treatment,fasting blood glucose,fasting insulin and ISI were significantly lower than before treatment (t =4.45,4.83,6.74,6.61,4.48,4.93,all P <0.05)and A group after treatment(t =4.23,448,5.24,515,409,3.95,all P <0.05),and the differences were statistically significant,and before and after treatment the total cholesterol,triglyceride,high density lipoprotein cholesterol and low density lipo-protein cholesterol levels among the three groups had no statistical significance;the level of uric acid of C group after treatment(282.04 ±81.31)μmol/L was significantly lower than that in A group and B group(t =4.94,4.68,all P <0.05).Conclusion Valsartan combined with amlodipine can effectively reduce the community elderly patients with primary hypertension in patients with diabetes mellitus blood pressure levels,promote the stability of blood glucose level,improve the uric acid metabolism and on renal function have protective effect.

Lung cancer and chronic obstructive pulmonary disease (COPD) are two high-mortality diseases in the world.Numerous epidemiological studies have demonstrated that presence of COPD increases the risk of lung cancer.Habitual cigarette smoking frequently develops lung cancer as well as COPD,However the links between the two diseases should be more than smoking alone.The underlying mechanisms may include genetic predisposition,inflammation and cell injury,oxidative and noxious stress,extracellular matrix and proteinases,some of which might represent the targets for chemoprevention or chemotherapy.

OBJECTIVE: To observe the effects of naoluotong on dogs' cerebral blood flow. METHODS:The anaesthetized dogs were randomly divided into naoluotong (which was subdivided into high, medium and low dose subgroups) group, antigeron positive control group, naoxuekang group, and blank control group with 6 dogs in each group. The internal carotid artery flow (ICAF), blood pressure (BP), electrocardiogram (ECG) and heart rates of the dogs were determined at different time after administration with drugs. RESULTS:As compared with the blank control group, the high and medium dose of naoluotong could significantly increase dogs' cerebral blood flow and reduce cerebral vascular resistance yet without significant influence on arterial blood pressure, heart rates and ECG. CONCLUSION: Naoluotong can improve cerebral blood circulation.

ABSTRACT:Objective To observe the influence of Osthole on cerebral ischemia-reperfusion injury and its acting mechanism.Methods We randomly divided 50 SD rats into sham (Sham)group,ischemia-reperfusion injury (IRI)group and Osthole (25,50,and 100 mg/kg)(Osthole)groups (n=10).The neurological symptoms, extent of cerebral infarction and cerebral water content were evaluated by physical approach.The activities of ROS and ATP were examined by the kit;the mitochondrial membrane potential (MMP ) was measured by flow cytometry.The expressions of Bax,Bcl-2,Caspase3,clevage-Caspase3,Caspase9,clevage-Caspase9,cytoplasmic AIF and cytochrome C were measured by Western blotting.Results Compared with those in sham group,the extent of cerebral infarction and cerebral water content,changes of neurological symptoms,activities of ROS,and expressions of clevage-Caspase3 ,clevage-Caspase9 ,Bax,cytoplasmic AIF and cytochrome C in IRI group were significantly increased (P<0.05).However,the activities of ATP,expressions of Caspase3,Caspase9,Bcl-2 and MMP,and ATP activity were decreased (P<0.05).Compared with those in IRI group,the extent of cerebral infarction and cerebral water content,changes of neurological symptoms,activities of ROS,and expressions of clevage-Caspase3 ,clevage-Caspase9 ,Bax,cytoplasmic AIF and cytochrome C in Osthole group were significantly decreased (P<0.05).But the activities of ATP,expressions of Caspase3,Caspase9,Bcl-2 and MMP,and ATP activities were increased (P < 0.05 ). Conclusion Osthole pretreatment can attenuate cerebral ischemia-reperfusion injury,which is associated with suppressing mitochondria-mediated apoptosis.

We only prolongated the course of shock from 2h to 5h, without predi- sposing the dogs. At 5h after hemorrhagic shock, the experimental results were asfollows: The ultrastructural damages were not only detected in the lung but also in theheart, liver, intestine and kidney etc. Major pathological lesions were: swelling of paren-chymal cells in various organs, vacular degeneration, and de-connection of cells. The laterwas shown as disintegration of hepatocyte-conjunction and disappearance of microvilli. Theorganelles of various cells ruptured to different degrees, for example, mitochondria swelledand its crista dissolved, endoplasmic reticulum dilated and de-granulated. In addition, thefibril of cardiac muscle thinned and dissolved, the capillary endothelial tight-conjunctionsof lung and intestine ruptured etc. The quantity of entero-endotoxin in plasma increasedin accordance with prolongation of shock, and its quantity was most abundant in portalvein, the next was artery and the last was hepatic vein. All experimental results showedthat the entero-endotoxin was related to the changes of ultrastructure of various organs.

Objective Establish a method for qualitative and quantitative analysis of paraquat dichloride in organs in rat by UPLC-MS/MS and study the rat animal model poisoned by intragastric administration of paraquat dichloride to investigate the postmortem distribution of paraquat dichloride in poisoning death rat. Methods The rats were given an intragastric administration of 1/2LD50 Paraquat dichloride. The rats were dissected at 0.5h, 2h, 4h, 8h, 12h, 24h, 48h, 72h respectively after the intragastric administration. The specimens of -the heart, liver, spleen, lung, kidney, brain, muscle, bladder and stomach-were collected and analyzed immediately. Qualitative and quantitative analysis were performed by UPLC-MS/MS. Results Within 4h, stomach is the main distribution organ. The content of paraquat dichloride is the highest in stomache and relatively low in other organs. The concentration of organization except stomach changed little within 4h. The concentration of stomach has a sharp decline after 4h. The concentration in organs except stomach has a sharp rise after 4h. There is a significant difference(P<0.05) between each organs and brain. Conclusion There was a postmortem maldistribution of paraquat dichloride in poisoning death rats and the concentration in organs changes with time. The analysis method of UPLC-MS/MS and postmortem distribution of paraquat dichloride can be applied to the forensic identification of paraquat dichloride poisoning death and provide direction for delete this part toxicology analysis.

AIM To study protective effect of [D-Ala~2, D-Leu~5]-enkephalin (DADLE) against hydrogen peroxide (H_2O_2) induced myocardial cell injury and its possible mechanisms. METHODS Myocardial cells were isolated from neonatal rats and cultured for 48 h. Then the cells were randomly assigned into normal control, H_2O_2（200 μmol·L~(-1)）, H_2O_2+DADLE(1 μmol·L~(-1)), H_2O_2+DADLE +naltrindole(10 μmol·L~(-1)) and H_2O_2+DADLE +U0126(10 nmol·L~(-1)) groups and cultured for another 48 h.[~3H]TdR incorporation assay and flow cytometry were used to measure the cell proliferation and apoptosis rate. The lactate dehydrogenase (LDH) activities in culture supernatant measured by using LDH activity kit. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in cells were measured with xanthine oxidase method and color reaction of thiobarbituric acid, respectively. The expressions of extracellular signal-regulated kinase (ERK) and phosphorylated-ERK (p-ERK) were observed with Western blot. RESULTS ① Compared with normal control group, the incorporation of [~3H]TdR in myocardial cells of H_2O_2 group was significantly lower, apoptosis rate was higher, LDH activity and MDA content in cells were higher, while SOD activity in cells was lower. In addition, the ratio of IA_( p-ERK) /IA_( ERK) was decreased. ② Compared with H_2O_2 group, the incorporation of ［3H］TdR in H_2O_2+DADLE group was significantly higher, apoptosis rate was lower, LDH activity and MDA content in cells decreased, while SOD activity increased significantly. The ratio of IA_( p-ERK) /IA_( ERK) was increased. ③ δ-Opioid receptor antagonist naltrindole and ERK antagonist U0126 inhibited this effect of DADLE on the above index changes induced by H_2O_2. CONCLUSION The δ-opioid receptor has protective effect against H_2O_2-induced myocardial cell injury, and its possible mechanism may be related to its promotion of antioxide capacity and ERK phosphorylation.

Objective To investigate the effect of emulsified isoflurane preconditioning on postsynaptic density protein 95 (PSD95) activation in brain during focal cerebral ischemia-reperfusion (I/R)injury in rats.Methods Thirty-two pathogen-free male SD rats weighing 280-300 g were randomly divided into 4 groups (n =8each): sham operation group(group S),group I/R,emulsified isoflurane group(group EI) and lipid emulsion group(group LE).Focal cerebral I/R was induced by middle cerebral artery occlusion for 2 h followed by reperfusion.8％ emulsified isoflurane 10.5 ml/mg or 30％ lipid emulsion 10.5 ml/mg was injected intraperitoneally at 24h before I/R in groups EI and LE respectively.The neurologic deficit score (NDS) was evaluated at 6 h of reperfusion and then 4 rats were sacrificed,and brains were removed for determination of phosphorylatied PSD95 (pPSD95) expression in ischemia cortex and hippocampus by Western blot.Four rats were sacrificed at 24 h of reperfusion and then their brains were removed for determination of infarct volume percentage.Results NDS,infarct volume percentage and pPSD95 expression in ischemia cortex and hippocampus were higher in groups I/R,EI and LE than in group S( P ＜ 0.01 ).NDS,infarct volume percentage and pPSD95 expression in ischemia cortex and hippocampus were lower in group EI than in group I/R( P ＜ 0.05).There was no significant difference in NDS,infarct volume percentage and pPSD95 expression between groups I/R and LE(P ＞ 0.05).Conclusion Emulsified isoflurane preconditioning can attenuate focal cerebral I/R injury in rats by inhibiting PSD95 activation in brain.

ObjectiveTo investigate the effects of emulsified isoflurane preconditioning on the expression of platelet-activating factor (PAF) and PAF receptor during focal cerebral ischemia-reperfusion (I/R) in rats.MethodsThirty-two healthy adult male SD rats weighing 250-300 g were randomly divided into 4 groups ( n =8each):group sham operation (group S); group I/R; group emulsified isoflurane preconditioning( group EI) and group lipid emulsion (group LE).Focal cerebral I/R was induced by 2 h occlusion of middle cerebral artery followed by reperfusion in groups I/R,EI and LE.8％ emulsified isoflurane 10.5 ml/kg and 30％ lipid emulsion 10.5 ml/kg were injected intraperitoneally at 24 h before cerebral ischemia in groups EI and LE respectively.The neurologic deficit score (NDS) (0 =no deficit,4 =unable to control) was evaluated at 12 h of reperfusion.Venous blood samples were collected for measurement of plasma PAF concentration.The animals were then sacrificed and their brains removed for determination of infarct size (by TTC staining) and PAF receptor expression in hippocampus and cerebral cortex (by Western blot).ResultsFocal cerebral I/R significantly increased NDS,the infarct size,plasma PAF concentration and PAF receptor expression in cerebral cortex and hippocampus in group I/R as compared with group S.Emulsified isoflurane preconditioning significantly attenuated the focal cerebral I/R induced above changes in group EI as compared with group I/R,but there was no significant difference between groups I/R and LE.ConclusionEmulsified isoflurane preconditioning can attenuate focal cerebral I/R injury by inhibiting PAF and PAF receptor expression.

By tracing of ~(75)Se-Na_2SeO_3 incubating and irrigating of the isolated myocardial slices of rats, the numeric relationship between the free selenics in the serum and the serum sdenics, the sodium sdenite doses injected were observed; the absorption of the frce selenics and the serum selenics was compared; the setenics metabolic rate and quantities of the myocardial tissue in different duration after injecting of selcnite, the effect of selenics concentration to the participating were calculated, It is suggested that there is a very close relationship between the free selenics and the selenium metabolism in the myocardium; the ratio betwen the values of the free selenics and the serum selenics may become a stable indicator of the selenium metabolism; the free selenics in the serum may be where the important mediates of selenium metabolism are.