The present experiments were designed to investigate the effects of atriopeptin I on different vascular smooth muscles.Isometric tension was recorded from spiral strips of human umbilical arteries, gastro-epiploica dextral arteries, rat and rabbit aorta. Atriopeptin H showed a potent inhibitor on the contraction induced by noradrenaline ( 3tmol/l), Serotonin ( lnmol/1), hista-mine ( 10M-mol/l ) and phenylephrine ( l(imol/l)in the strips of rat and rabbit aorta, but not on the contraction induced by the above-mentioned drugs and KC1 (80mmol/l), prostaglandine F2a ( 10umol /I) in umbilical and gastroepiploica dextral arteries of human beings. Sodium nitroprussids showed also a potent antagonist on the contraction induced by noradrenaline ( 3 M-mol/1) serotonin ( 1imol/l), histamine (10imol/1) and prostaglandine F2a (10nmol/l) in the strips of umbilical arteries.lt produced concentration-dependent inhibition of the contraction induced by noradrenaline.It could remarkably decrease the resting tension of the strips.The present results suggest that atriopeptin I exhibits a similar vasodilator profile in rat and rabbit aorta as that found for sodium nitroprusside in the human umbilical arteries.The ineffectiveness of atriopeptin I on human umbilicalj and gas-troepiploica dextral arteries is in marked contrast to the effectiveness of sodium nitroprusside in the human umbilical arteries, indicating that the action of atriopeptin f possesses species difference.

OBJECTIVE: To promote the development of clinical pharmacy and improve the social efficacy of ADR monitoring so as to ensure safe and rational use of drugs.METHODS: The current status of Chinese ADR monitoring system and the problems faced in the development of ADR monitoring were analyzed by means of literature review,contrasting analysis,and data reduction etc.RESULTS & CONCLUSION: There are many problems existed in the current ADR monitoring,for instance: the regulations system of ADR monitoring is unsound,the monitoring technology is weak;the cognition level of many medical workers is still very low etc.It is urgently needed to intensify propaganda on ADR monitoring,strengthen ADR monitoring,develop technological system of monitoring,set up expert database and train professional talents.

AIM:To investigate the effect of non-mitogenic human acidic fibroblast growth factor(nm-haFGF)on renal ischemia-reperfusion injury in rats.METHODS:Rat renal ischemia-reperfusion(I/R)injury was produced by removing the left kidney and subsequently clamping the right renal artery for 60 min followed by reperfusion for 24 h.5 min after reperfusion.different doses of nm-haFGF and haFGF(as positive control)were injected by lingual vein.24 h later,the samples of blood,urine and kidney were collected and the contents of malondialdehyde(MDA),blood urea nitrogen(BUN),creatinine(Cr)and superoxide dismutase(SOD)activity were detected.Histopathological changes were also observed.RESULTS:In the serum,SOD activity of all the nm-haFGF groups and the haFGF group increased significantly while the content of MDA decreased dramatically compared with the model group;The content of BUN and Cr aland haFGF group rose significantly compared with the model group,while MDA decreased dramatically.Histological examination showed that nm-haFGF markedly attenuates the renal edema,brush border's defluvium and cell necrosis induced by ischemia-reperfusion.CONCLUSION:nm-haFDF could resist the renal injury induced by ischemia-reperfusion in rats.

AIM To test if "adventitium-derived relaxing factor"(ADRF) possesses species- and tissue-specificity and make preliminary research on proteins separated from the bath solution. METHODS Record the tension of aortic ring with and without periadventitial fat, induced by phenylephrine(Phe) and analyze the proteins extracted from the bath solution with SDS-PAGE electrophoresis. RESULTS ① In Sprague-Dawley rats, the concentration-response curve of Phe to rings without the periadventitial fat shifted to rightward, as compared to the curve of the intact aortic rings, which means periadventitial fat can reduce the contraction induced by Phe. The same phenomena as the above could be found in aortic ring of Wistar rats, guinea pigs, and rabbits. ② Moreover, the contraction induced by Phe was obviously reduced by moving adipose tissue from greater omentum into the bath solution. ③ The release of ADRF was strongly reduced by 10 μmol·L-1 genistein (tyrosine kinase inhibitor). But the effect of existed ADRF could not be counterposed by genistein. ④ Five protein bands were separated from the bath solution, with relative molecular mass 74.0, 59.8, 54.4, 28.7 and 13.8 ku. CONCLUSION ① ADRF is a non-species specific factor. ② The entire name of ADRF should change from "adventitium-derived relaxing factor" to "adipocyte-derived relaxing factor". ③ Some proteins which may include ADRF are separated from the bath solution.

Aim To explore the effects of lipoteichoic acid (LTA) induced delayed preconditioning (PC) on hypoxia-reoxygenation (H/R) injury of cultured human coronary artery endothelial cells (HCAECs), and to investigate the potential role of endogenous nitric oxide (NO) participated in the protective mechanism. Methods HCAECs were incubated for 2 h in a hypoxic atmosphere and reoxygenated for 4 h in a normoxic atmosphere. The delayed PC was induced by pretreatment with LTA assessed by the percentage of cellular injury with Trypan blue exclusion and by the amount of lactate dehydrogenase (LDH) in culture media. The NO level of the culture media was measured detect the expression of eNOS mRNA by RT-PCR method after cells were recovered from different points.Results LTA pretreatment significantly decreased the percentage of the killed cell and the concentration of LDH in media. Also, LTA pretreatment obviously raised the concentrations of NO in culture media. The protective effects of LTA were abrogated by pretreatment with N-monomethyl-L-arginine (L-NMMA).Moreover, the expression of eNOS mRNA was significantly upregulated after HCAECs exposure to LTA for 4 h following 2 h or 4 h recovery. Conclusion LTA could induce the delayed protection against H/R induced endothelial injury and dysfunction of cultured HCAECs. NO produced by eNOS acts initially as a trigger and subsequently as a mediator of delayed PC.

The effects of phorbol-12,13-dibuterate (PDBu) on total sodium current (I(Na)-total), tetrodotoxin-resistant sodium current (I(Na)-TTXr), 4-AP-sensitive potassium current (I(A)) and TEA-sensitive potassium current (I(K)) in trigeminal ganglion (TG) neurons were investigated. Whole-cell patch clamp techniques were used to record ion currents in cultured TG neurons of rats. Results revealed that 0.5 micromol/L PDBu reduced the amplitude of I(Na)-total by (38.3+/-4.5)% (n=6, P<0.05), but neither the G-V curve (control: V (0.5)=-17.1+/-4.3 mV, k=7.4+/-1.3; PDBu: V (0.5)=-15.9+/-5.9 mV, k=5.9+/-1.4; n=6, P>0.05) nor the inactivation rate constant (control: 3.6+/-0.9 ms; PDBu: 3.6+/-0.8 ms; n=6, P>0.05) was altered. 0.5 micromol/L PDBu could significantly increase the amplitude of I(Na)-TTXr by (37.2+/-3.2)% (n=9, P<0.05) without affecting the G-V curve (control: V (0.5)=-14.7+/-6.0 mV, k=6.9+/- 1.4; PDBu: V (0.5)=-11.1+/-5.3 mV, k=8.1+/-1.5; n=5, P>0.05) or the inactivation rate constant (control: 4.6+/-0.6 ms; PDBu: 4.2+/-0.5 ms; n=5, P>0.05). 0.5 mumol/L PDBu inhibited I(K) by (15.6+/-5.0) % (n=16, P<0.05), and V (0.5) was significantly altered from - 4.7+/-1.4 mV to -7.9 +/-1.8 mV (n=16, P<0.05). I(A) was not significantly affected by PDBu, 0.5 mumol/L PDBu decreased I(A) by only (0.3+/-3.2)% (n=5, P>0.05). It was concluded that PDBu inhibited I(Na)-total but enhanced I(Na)-TTXr, and inhibited I(K) without affecting I(A). These data suggested that the activation of PKC pathway could exert the actions.

In order to evaluate the neuroprotective effect of Rosiglitazone Maleate (RSG) against brain ischemic injury, the effects of Rosiglitazone Maleate on the inflammation following cerebral ischemia/reperfusion were investigated. Focal cerebral ischemia was induced by the intraluminal thread for cerebral middle artery (MCA) occlusion. Rosiglitazone Maleate at concentrations of 0.5, 2 and 5 mg/kg was infused by intragastric gavage twice immediately and 2 h after MCA occlusion, respectively. The effects of Rosiglitazone Maleate on brain swelling, myeloperoxidase and interleukin-6 mRNA level in brain tissue after MCA occlusion and reperfusion were evaluated. The results showed that as compared with the model control group, RSG (0.5 mg/kg) had no significant influence on brain swelling (P>0.05), but 2 mg/kg and 5 mg/kg RSG could significantly alleviate brain swelling (P<0.05). All different doses of RSG could obviously reduce MPO activity in brain tissue after MCA occlusion and reperfusion in a dose-dependent manner. RSG (0.5 and 2 mg/kg) could decrease the expression levels of IL-6 mRNA in brain tissue after MCA occlusion and reperfusion to varying degrees (P<0.05) with the difference being significant between them. It was concluded that RSG could effectively ameliorate brain ischemic injury after 24 h MCA occlusion and inhibit the inflammatory response after ischemia-reperfusion in this model.

In order to investigate the antiviral effect of chinonin against Herpes simplex virus (HSV), the encephalitis model in mice and skin infection model in guinea pigs were established by HSV- I and HSV-II infection respectively. Acyclovir was used as the positive reference drug to evaluate the antiviral capacity of chinonin. Chinonin showed an obvious therapeutic effect on encephalitis in mice at doses of 25 and 50 mg/kg. At both dosages, chinonin demonstrated stronger protection than acyclovir (1 and 5 mg/kg) to the infected mice from death. It was also found that chinonin could treat the skin infection in guinea pigs effectively. The therapeutic effect of chinonin was similar to that of acyclovir (5 mg/kg) at 25 mg/kg but obviously better than that at 50 and 75 mg/ kg. In conclusion, chinonin is a potential candidate for the treatment against HSV.

AIM: To investigate the effect of non-mitogenic human acidic fibroblast growth factor(nm-haFGF) on renal ischemia-reperfusion injury in rats.METHODS: Rat renal ischemia-reperfusion(I/R) injury was produced by removing the left kidney and subsequently clamping the right renal artery for 60 min followed by reperfusion for 24 h.5 min after reperfusion,different doses of nm-haFGF and haFGF(as positive control) were injected by lingual vein.24 h later,the samples of blood,urine and kidney were collected and the contents of malondialdehyde(MDA),blood urea nitrogen(BUN),creatinine(Cr) and superoxide dismutase(SOD) activity were detected.Histopathological changes were also observed.RESULTS: In the serum,SOD activity of all the nm-haFGF groups and the haFGF group increased significantly while the content of MDA decreased dramatically compared with the model group;The content of BUN and Cr also decreased wherever in serum or in urine;In renal tissue,SOD activity in nm-haFGF 20 ?g/kg group,40 ?g/kg group and haFGF group rose significantly compared with the model group,while MDA decreased dramatically.Histological examination showed that nm-haFGF markedly attenuates the renal edema,brush border's defluvium and cell necrosis induced by ischemia-reperfusion.CONCLUSION: nm-haFDF could resist the renal injury induced by ischemia-reperfusion in rats.

AIM: To study the protection of extract of Radix Atragali composite against acute hepatic injury. METHODS: Fed with the extract of Radix Atragali composite, m ice were injected with D-galactosamine intraperitoneally (800 mg/kg) and rats were i njected with carbon tetrachloride hypodermically (5 mL/kg) to induce acute hepat ic injury on the 8th day. ALT, AST and bilirubin in serum were examined. Patholo gical changes of liver tissue were observed. RESULTS: Compared with model group, activities of ALT and AST, c oncentrations of bilirubin were markedly decreased and pathological scores also showed that degeneration and necrosis of hepatic cell were lighter in the the ex tract of Radix Atragali composite treatment group. CONCLUSION: The extract of Radix Atragali composite attenuat es hepatic injury induced by D-galactosamine or carbon tetrachloride.