目的 探討培哚普利降壓治療對預防高血壓合并腦卒中患者并發癥的研究.方法 對155例既往有腦卒中病史的輕中度高血壓病患者隨機分組,進行三年的培哚普利及安慰劑的雙盲對照臨床試驗,觀察三年的治療組及安慰劑組的血壓、心腦血管并發癥的發生率及病死率,在研究結束時給予連續3日動態血壓監測(ambulatory blood pressure monitoring,ABPM).結果 與安慰劑組比較,治療組3日動態血壓監測示血壓控制滿意,三年心腦血管并發癥的發生率和死亡率(分別為6.85%和2.74%)明顯低于安慰劑組(17.10%和9.21%).結論 培哚普利降壓有效、平穩、持久,持續降壓治療對預防高血壓合并腦卒中患者心腦血管并發癥具有重要作用.
摘要:目的: 比較咪達普利與培哚普利對原發性高血壓患者的的降壓效果和不良反應。 方法 :將入選的60例1～2級高血壓病患者,隨機分為2組,咪達普利組,每日晨起口服咪達普利(5～10 mg,1次/d),培哚普利組,每日晨起口服培哚普利(4～8 mg,1次/d)。治療4周,觀察2組治療前、后的血壓,記錄不良反應。 結果 :經治療后咪達普利與培哚普利組血壓均明顯下降(Plt;0.05),組間差異無統計學意義(P＞0.05);總不良反應發生率咪達普利組16.8%,培哚普利組20%,而咪達普利組的咳嗽發生率為6.8%,培哚普利組為16.8%。 結論 :咪達普利和培哚普利均能有效降壓,二者降壓效果相似,但咪達普利的咳嗽發生率較低。Abstract: Objective: To compare the antihypertensive efficacy and safety of imidapril versus peridopril in patients with essential hypertension. Methods : Selected 60 patients with mild to moderate essential hypertension, in which divided two groups by random.They were administered imidapril 5～10 mg once daily or and peridopril 4～8 mg once daily for 4 weeks. During the curative period of 4 weeks, the antihypertensive efficacy and adverse reaction were observed. Results :The blood pressure drecreased prominently in both groups after four weeks treament(Plt;0.05), but there was no significant difference in antihypertensive efficacy between the two groups(P＞0.05). The occurrence of the total adverse reaction in imidapril and peridopril groups was 16.8% and 20%, respectively, while the occurrence of the cough in two groups was 6.8% and 16.8%, respectively. Conclusion :Both imidapril and peridopril exert favourable and similar hepotensive effect, however the cough occurrence of imidapril is lower than that of peridopril.
目的觀察培哚普利對慢性阻塞性肺疾病(簡稱慢阻肺)大鼠肺功能及肺組織磷酯酰肌醇3-激酶(PI3K)的影響,為培哚普利治療慢阻肺提供科學依據。 方法將60只雄性SD大鼠隨機分為正常對照組、模型組及培哚普利干預組,每組各20只。采用兩次氣管滴注脂多糖(LPS)加煙熏的方法建立慢阻肺大鼠模型,第28 d時檢測大鼠肺功能和肺組織中PI3K表達水平,HE染色觀察大鼠肺組織病理改變。 結果模型組大鼠肺組織HE染色符合慢阻肺的病理改變,培哚普利干預組肺氣腫程度較慢阻肺組大鼠減輕;模型組、干預組大鼠的肺功能與對照組比較均有下降,模型組的每分鐘呼氣量(VE)、最大呼氣流量(PEP)和0.3 s用力呼氣容積(FEV0.3)較干預組下降更為顯著,差異均有統計學意義(P<0.01或P<0.05);模型組、干預組肺組織中PI3K表達水平與對照組比較均有上升,差異均有統計學意義(P<0.01或P<0.05),但模型組較干預組上升更為顯著,差異均有統計學意義(P<0.05)。 結論培哚普利能明顯改善慢阻肺大鼠肺功能,其機制可能是通過下調肺組織中PI3K的表達水平來實現的。