【正文】
neous hypertension rats (SHR). Method: 12 SHR were divided into two groups. We collected blood samples from each of rat . Study group: administration of CoQ10 (20mg/day)。第十六天先測定血壓,然后注射拉貝洛爾,10min后再測血壓。動(dòng)物麻醉處死,心臟采血,并取心臟稱重。 control group: placebo (physiological saline), for 15 days. We measured Bp and Hr every 5 days. 15th day: collection of the second blood sample. 16th day: measurement of Bp and injection of Labetalol and 10 minutes later, we measure Bp. We anesthetized the rats, collected the third blood sample from heart and weigh rats’ hearts. Serumal items: SOD and MDA. Results: after 15 days’ administration, Bp of the rats in study group dropped significantly (p) while that of control group were unchanged. After the injection of oneforth of the minimum dose of labetalol, Bp of the rats in study group dropped more rapidly than that of control group. But the concentration of the items in serum didn’t change greatly. Conclusion: CoQ10 has a hypotensive effect. It can protect the high risk people and reduce the dose of regular medication (hypotensor). The mechanism of CoQ10 is independent from its role in antilipid peroxydation. [Key Word] idiopathic hypertension。新近發(fā)現(xiàn)脂質(zhì)過氧化反應(yīng)可能參與了高血壓發(fā)生和發(fā)展的病理過程[9]。在連續(xù)三天測定血壓的基礎(chǔ)上,取第二天和第三天的血壓均值作為基礎(chǔ)血壓。將制備得到的血清置于eppendorf管中,20℃保存?zhèn)溆谩?0分鐘后,測定其血壓。血清學(xué)指標(biāo)檢測 實(shí)驗(yàn)組和對(duì)照組三次采集和制備的血清于同一天進(jìn)行SOD,MDA檢測(試劑盒均購自南京建成生物工程研究所)。結(jié) 果1.輔酶Q10的降壓效果觀察 實(shí)驗(yàn)組動(dòng)物連續(xù)服用輔酶Q10 15天,對(duì)照組動(dòng)物服用安慰劑(生理鹽水)15天內(nèi),動(dòng)物血壓如圖1所示。實(shí)驗(yàn)組:p,對(duì)照組:p,表明輔酶Q10有降血壓作用。圖3 連續(xù)灌胃15天后,兩組大鼠心重比較 (n=3)3. 輔酶Q10和拉貝洛爾的聯(lián)合作用 確定拉貝洛爾注射劑量實(shí)驗(yàn)。血清中SOD濃度 服用輔酶Q10前后,大鼠血清SOD濃度如表5所示,實(shí)驗(yàn)組和對(duì)照組十五天后其均值可見明顯變化,但因個(gè)體數(shù)太少使得變異度相對(duì)較大,無統(tǒng)計(jì)學(xué)意義。IgarashiT等人[11]觀察了輔酶Q10對(duì)不同高血壓動(dòng)物模型(特別是自發(fā)性高血壓大鼠SHR)的作用,實(shí)驗(yàn)發(fā)現(xiàn):輔酶Q10對(duì)正常大鼠沒有降壓作用;但在不同的高血壓動(dòng)物模型中,口服輔酶Q10對(duì)抑制血壓升高或降低血壓有效。在我國,也有人[6]得出了貝那普利(血管緊張素轉(zhuǎn)換酶抑制劑)與輔酶Q10聯(lián)合用治療原發(fā)性高血壓比單用貝那普利效果好的結(jié)論。其降血壓機(jī)制為:(1)CoQH2與ADPperferryl ion 作用ADPFe3+O2● + CoQH2 → ADPFe2+ + H2O2 + CoQ(2 ) CoQH2直接清除O2●2 O2● + CoQH2 → H2O2 + O2 + CoQ(3 ) CoQH2脂自由基或脂過氧基反應(yīng)2L● + CoQH2 → 2LH + CoQ2LOO● + CoQH2 → 2LOOH + CoQ也有證據(jù)表明超氧陰離子使NO失活有關(guān),即氧化作用加強(qiáng)導(dǎo)致NO損傷,氧自由基是NO損傷的誘導(dǎo)劑,超氧陰離子及氧化型LDL使內(nèi)源性舒張因子NO失活,而使內(nèi)皮細(xì)胞受損[10]。2. 年齡因素對(duì)于高血壓的形成機(jī)制可能存在的影響。由此,作者提出:①青年高血壓患者的血壓形成機(jī)制不能單純用脂質(zhì)過氧化來解釋;②脂質(zhì)過氧化雖然是高血壓進(jìn)展演變過程中一個(gè)不可忽視的因素,但是,單純的脂質(zhì)過氧化可能無法引發(fā)高血壓的形成,必須要首先存在一個(gè)誘因,使得體內(nèi)抗氧化機(jī)制嚴(yán)重失調(diào),從而進(jìn)一步誘發(fā)大量脂質(zhì)過氧化物對(duì)血管內(nèi)皮細(xì)胞的損害,使血壓的升高變得更加明顯和嚴(yán)重。我們發(fā)現(xiàn)12號(hào)大鼠死于腦溢血,全身無明顯病變。 Nutrition Research. 44(4):48796, 1974.[3]Folkers K. Drzewoski J. Richardson PC. Ellis J. Shizukuish