目的 探討培哚普利降壓治療對預(yù)防高血壓合并腦卒中患者并發(fā)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(fā)癥的發(fā)生率及病死率,在研究結(jié)束時給予連續(xù)3日動態(tài)血壓監(jiān)測(ambulatory blood pressure monitoring,ABPM).結(jié)果 與安慰劑組比較,治療組3日動態(tài)血壓監(jiān)測示血壓控制滿意,三年心腦血管并發(fā)癥的發(fā)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(jié)論 培哚普利降壓有效、平穩(wěn)、持久,持續(xù)降壓治療對預(yù)防高血壓合并腦卒中患者心腦血管并發(fā)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(fā)性高血壓患者的的降壓效果和不良反應(yīng)。 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(yīng)。 結(jié)果 :經(jīng)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(tǒng)計學(xué)意義(P＞0.05);總不良反應(yīng)發(fā)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(fā)生率為6.8%,培哚普利組為16.8%。 結(jié)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(fā)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(xué)依據(jù)。 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(yù)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(jié)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(yù)組肺氣腫程度較慢阻肺組大鼠減輕;模型組、干預(yù)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(yù)組下降更為顯著,差異均有統(tǒng)計學(xué)意義(P<0.01或P<0.05);模型組、干預(yù)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(tǒng)計學(xué)意義(P<0.01或P<0.05),但模型組較干預(yù)組上升更為顯著,差異均有統(tǒng)計學(xué)意義(P<0.05)。 結(jié)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(diào)肺組織中PI3K的表達水平來實現(xiàn)的。