Intravenous injection of l-stepholildine (SPD) 2.5, 10 and 40 mg/kg decreased blood pressure(BP ) by 30, 40 and 55% respectively in anesthetized dogs. SPD also decreased BP in anesthetized rats (0.5mg/kg iv, by 29% and 2-50 mg/kg injected into duodenum, by 17-36%) and rabbits (2.5 mg/kg iv, by 24%). It could inhibit the pressor reflexes induced by occluding carotid, stimulating vagus Or sciatic nerve. Furthermore, SPD 2.5 mg/kg injected into fourth cerebroventricle of dog decreased BP by 20%, and in pithed rats SPD 10-40 mg/kg iv depreased BP by 7-40%. These results indicate that both central and peripheral mechanisms are involved in the hypotens-ive action of SPD and the peripheral seems to be more important. As showed in previous papers the effect of SPD on ?-adrenoceptors may be one of the chief mechanisms of the hypotensive action induced by SPD.

The Prescription for Pharmacoeconomic Analysis (PFPA) of New Zealand was firstly published in 1999. The original version was reviewed in 2004 and version 2, approved and published in 2007, is the living document. The main purpose for this guideline is to provide an overview of the methods PHARMAC (Pharmaceutical Management of Agency) uses when conducting cost-utility analysis. Compared with version 1, version 2 involved and discussed the most frequently mentioned issues in pharmacoeconomic guidelines around the world. This paper describes the distinguishes between version 1 and 2, the advantages of version 2 as well as the amendments that will be made in PHARMAC's future work, in order to provide meaningful advice for standardizing and documenting methods in China
Costs and Cost Analysis ; Economics, Pharmaceutical ; Humans ; New Zealand

Objective To investigate the effect of dexmedetomidine (DEX) on the reduction of brain injury induced by lung ischemia/reperfusion (I/R) in mices through inhibiting excessive endoplasmic reticulum stress response (ERS).Methods Fifty healthy SPF male C57BL/6J mices,weighing 20-24 g,aged 8-10 weeks,were divided into 5 groups (n =10 each) using a random number table:sham operation group (sham group),lung ischemia/reperfusion group (I/R group),atipamezole goup (Atip group),dexmedetomidine group (DEX group),dexmedetomidine plus atipamezole group (DA group).The model of lung I/R injury was established by clamping the left hilum of lung for 30 min followed by reperfusion for 180 min.In Atip,DEX and DA groups,atipamezole 250 μg/kg,dexmedetomidine 20 μg/kg and dexmedetomidine 20 μg/kg plus atipamezole 250 μg/kg were injected intraperitoneally,respectively,at 30 min before modeling,other procedures were as the same as the I/R group.At 180 min of reperfusion,the animals were sacrificed and the brain tissues were harvested for the observation of morphological changes.The Caspase-3 activity and the apoptosis index of the brain cells were also determined.The levels of protein and mRNA expression of p-JNK,Caspase-12,CHOP and GRP78 in brain tissues were detected by Western blot and RT-PCR.The datas were analyzed using SPSS 19.0 software and multiple-group comparisons were performed using one-way ANOVA,and P ＜ 0.05 for the difference was statistically significant.Results Compared with the sham group,the Caspase3 activity and brain cell apoptosis index,the protein levels and mRNA expressions of p-JNK,Caspase12,CHOP,GRP78 were significantly increased (P ＜ 0.01),brain tissues had obvious damage in I/R,Atip,DEX and DA groups;compared with I/R,Atip and DA group,brain tissues damage was obvious reduced in DEX group,and the Caspase3 activity,brain cell apoptosis index,the protein levels and mRNA expression of p-JNK,Caspase12,CHOP in DEX group were significantly lower,and GRP78 expression increased significantly (P ＜ 0.01).Comparisons among I/R,Atip and DA groups,there were no significant differences in degree of brain injury,Caspase3 activity,brain cell apoptosis index,the protein levels and mRNA expressions of p-JNK,Caspase12,CHOP (P ＞ 0.05),while the expression of GRP78 in DA group was significantly increased (P ＜ 0.01).Conclusion DEX can effectively relieve the brain injury induced by lung I/R in mice,which may be associated with stimulation of α2 adrenergic receptor and inhibition of excessive endoplasmic reticulum stress response and reducing brain cell apoptosis.