In both clinical and animal experiments,it has been confirmed that the inflammation in heart is involved in the development of heart injury after the ischemia/reperfusion.However,the pro-inflammatory mechanism is extremely complicated.Recently,a growing number of reports indicates that many factors play their roles in the inflammation,such as cytokinemia,inflammatory cells,metabolic product of arachidonic acid and COX et al.They are released/presented in the region of myocardial ischemia/reperfusion and include both ischemic and secondary heart injury.

BACKGROUND: Total flavone of ginkgo biloba(TFG) can affect on free radical, but the effect on apoptosis induced by cerebral ischemia is unclear.OBJECTIVE: To study the inhibitory effect of TFG on apoptosis induced by cerebral ischemia.DESIGN: Completely randomized controlled experimental study based on experimental animals.SETTING: Department of pharmacology in a university.MATERIALS: Totally 24 SD rats in half genders with clean grade and body mass of(250 ± 50) g, were divided into 4 groups at random: sham-operation group, model group, TFG 40 rmg/kg group and TFG 80 mg/kg group (Certificate No. 01).METHODS: This study was completed in the Department of Pharmacology,Anhui Medical University during October 2001 and January 2002. Incomplete cerebral ischemia was made by ligating bilateral common carotid arteries(CCA) in rats. The cerebral injury was evaluated by brain edema. The apoptosis was determined by terminal deoxy-nucleotidyl transforase-mediated dUTP-digoxigenin nick end-labeling(TUNEL) and transmission electron microscopy (TEM) method. The DNA fragmentation analysis was measured with the diphenylamine reagent method.MAIN OUTCOME MEASURES: Major factor: Effect of TFG on ultrastructral alteration of apoptotic cerebral cortex cells; Secondary factor: Effect of TFG on DNA fragmentation induced by cerebral ischemia.RESULTS: Ligating of bilateral CCA markedly induced apoptotic cell in cerebral cortex. TFG 80 mg/kg significantly inhibited brain edema( P ＜ 0.05 )and decreased the numbers of apoptotic cells in cortex( P ＜ 0.01 ) and improved ultrastructral alteration of apoptotic cells; TFG 40, 80 rmg/kg also inhibited the increase of DNA fragmentation induced by cerebral ischemia (P ＜0.05, P ＜0.01).CONCLUSION: TFG has inhibitory effect on ischemia-induced apoptosis of cerebral cortex and improve the ultrastructual changes of apoptosis. Moreover,TFG can relieve the occurrence of edema of ischemic brain tissue and inhibit the increase of DNA section induced by cerebral ischemia.

Aim To observe the neuroprotective effect of sinomenine on hippocampal neurons from injury in-duced by oxygen glucose deprivation ( OGD ) and its underlying mechanism. Methods Hippocampal neu-rons were exposed to OGD for 4 h followed by 24 h re-oxygenation ( OGD-R) . Then cell viability was detec-ted by MTT. LDH release was detected by LDH kit. Cell apoptosis was detected by Hoechst stain. The ex-pression of Bax, Bcl-2 and caspase-3 were detected by Western blot. [ Ca2+] i of hippocampal neurons was detected by calcium imaging. Acid-sensing ion chan-nels ( ASICs ) current was detected by patch clamp technique. Results SN increased cell viability and reduced LDH release. SN also inhibited neuron apop-tosis and increased ratio of Bcl-2/Bax and reduced the expression of caspase-3 . OGD-induced increase of [ Ca2+] i was inhibited by SN. Furthermore, SN inhib-ited ASIC1 a current and also inhibited OGD induced increase of ASICs current in hippocampal neurons. Conclusion SN protects hippocampal neurons against OGD-R-induced injury. The inhibitory effect of SN on ASIC1 a and calcium overload was involved in the pro-tective effect of SN.

AIM　To study the role of 5-HT in antinocieption produced by intrathecal indomethacin (Ind) in mice. METHOD　The antinocieption of indomethacin was investigated on the tail immersion test in mice；the contents of 5-HT, 5-HAA were assayed with fluorescent method. RESULT　Dose-dependent antinocieption was observed following intrathecal administration of Ind 1.8 mg*kg-1, the effect could be obliterated when the animals were pretreated with cyproheptadine. After intrathecal administration of Ind, the content of 5-HIAA in the spinal cord of mice was significantly increased, but PG had no effect. CONCLUSION　The result imply that intrathecal indomethacin could produce antinocieption; this effect is mediated by 5-HT. PG does not participate in the action of 5-HT.

Objective To observe the protective effect of total flavone of Camellia (TFC)against cerebral ischemic injury.Methods Decapitation method and close hypoxia method were used to observe the effect of TFC on anoxic tolerance of mice and step down test was used to observe the effect of TFC on learning and memory; after ischemia, the content of malondialdehyde (MDA)and nitric oxide (NO)and the activity of lactate dehydrogenase (LDH)were detected. Rat models with acute incompletely cerebral ischemia were established by means of ligating right common carotid arteries and effect of TFC on cerebral water volume, permeability of cerebral vessels and cerebral histopathological changes were also observed.Results TFC prolonged the grasping time after decapitation and the survival time after anoxia in mice, and improve the learning and memory during the step down test. TFC decreased MDA and NO contents, counteracted the de creases of LDH activities in the mice cerebral cortex, reduced the water volume and permeability of cerebral vessels in ischemic rats and improve the cerebral hitstopathological changes. Conclusion TFC has protective effects against cerebral ischemic injury and the mechanism may be related to the inhibition of free radicals and NO production.

Aim To study protective effects of Total of flacone C(TFC) against cerebral ischemia-reperfusion injury.Methods Four-vessel occlusion method was used to make acute cerebral ischemia-reperfusion model. Rats were initiated by ischemia for 30 min followed by 40 min of reperfusion.The electroencephalography(EEG) during cerebral ischemia and reperfusion was recorded.The level of intracellular calcium ion concentration([Ca~(2+)]i) in cerebral cells after ischemia was measured by using a Ca~(2+) indicator Fura-2/AM.Superoxide dismutase(SOD),Glutathione peroxidase(GSH-Px),Lactate dehydrogenase(LDH),nitric oxide Synthase(NOS) activeties and Malondialdehyde(MDA),Nitric Oxide(NO)contents in the ischemia cerebral cortex were measured.Results TFC can improved the EEG change,significantly attenuated the decrease of the intracellular calcium ion concentration([Ca~(2+)]_i), remarkly increased GSH-Px,SOD and NOS activities in the cerebrum,inhibit the decrease of LDH activity and NO,MDA contents.Conclusion TFC has protective effects on cerebral ischemia-reperfusion injury,the mechanism may be related to attenuating free radical,[Ca~(2+)]i overload and NO.

AIM: To investigate the protective effects of total of flavone C (TFC) on acute cerebral ischemia in mice and focal cerebral ischemia in rats. METHODS: The occlusion of bilateral common carotid arteries with vagus nerves in mice was used for make the acute cerebral ischemia models. The survival time and the death rate were observed. The permanent occlusion of the proximal of the right middle cerebral artery (MCA) was used for make the focal cerebral ischemia models. The extent of neurological deficits was observed, and the infarct area was measured by NBT staining technique. The activity of LDH and the content of MDA and NO in the ischemic cerebral cortex were determined. RESULTS: TFC of 80 and 40 mg?kg -1 prolonged the survival time and decreased the death rate of mice with acute cerebral ischemia injury. TFC of 60, 30, and 15 mg?kg -1 ameliorated neurologic deficits score and the infarct size of rats with MCAO. CONCLUSION: TFC provides significant protective effects against cerebral ischemia injury.

AIM To observe the long-term toxicities of reteplase(Ret). METHODS Rat was administrated by injection of vein on 14 consecutive days to macaca fasicular. RESULTS Ret 8.0 MIU?kg -1 to macaca fasicular did not show any toxicity. In 25.0 MIU?kg -1 and 80.0 MIU?kg -1 of doses, RBC, HGB and HCT of blood have significantly decreased. Feces of hidden blood test also showed positive response in some animals, meanwhile, Ret could reduce the content of plasma total protein. But these changes could have recovery in restoration period. In addition, in 8.0?25.0?80.0 MIU?kg -1 doses, Ret could significantly lengthen bleeding time and clotting time. The obvious toxic changes of coefficient and pathology in Ret 8.0?25.0?80.0 MIU?kg -1 groups were not found. CONCLUSION 8.0 MIU?kg -1 is a safety dosage by injection of vein. 25.0,80.0 MIU?kg -1 doses have certain toxic actions, such as anemia and bleeding, but these toxic effects were reversible.

Objective To study the protective effects of total flavone C( TFC) on myocardial ischemia and to explore its mechanism.Methods Two kinds of models were established: mouse model of myocardial ischemia induced by means of clampi ng trachea and rat models of myocardial ischemia induced by pititrin.Results TFC at the concentrations of 80 and 40 mg/kg markedly prolonged the cardioelectric time after clamping the trachea.TFC at the concentrations of 60 and 30 mg/kg can ameliorate the changes of ST and T wave in rat models,reduce the MDA contents in the myocardium and the serum of rats and decrease the activity of LDH in the serum of rats.Conclusion TFC has protective effects on moyocardial ischemia and its mechanism may be related with the inhibition of lipid peroxidation.

OBJECTIVETo investigate whether transdermal scopolamine increased cardiac vagal activity in patients during the acute phase of myocardial infarction.

METHODS30 patients with a first acute myocardial infarction and preserved sinus rhythm who were on no drug that could influence the sinus node were randomly assigned to either treatment group or placebo group. Measures of heart rate variability (HRV) in patients given drug or placebo were obtained by digital 24 hour Holter recording before and after treatment. Baroreflex sensitivity was performed using the phenylephrine method.

RESULTSNo significant differences was found in the indices of the time domain and the frequency domain in both groups before treatment. Patients with transdermal scopolamine showed a significant increase in the standard deviation of normal RR intervals (SDNN), standard deviation of all five min mean normal RR intervals (SDANN), root mean square of differences of successive normal RR intervals (rMSSD), total power (TP, 0.000. - 0.40 Hz), low frequency peak (LF, 0.040 - 0.15 Hz), high frequency peak (HF, 0.15 - 0.40 Hz), and Baroreflex sensitivity after treatment (P < 0.05 - 0.01). These indices did not change in patients given placebo.

CONCLUSIONLow doses of transdermal scopolamine safely increase cardiac parasympathetic activity and improve autonomic indices in patients with acute myocardial infarction.

Administration, Cutaneous ; Adult ; Aged ; Baroreflex ; drug effects ; Dose-Response Relationship, Drug ; Female ; Heart ; innervation ; Heart Rate ; drug effects ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; physiopathology ; Scopolamine Hydrobromide ; pharmacology ; Vagus Nerve ; drug effects ; physiopathology