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作 者:张福琴[1] 李志超[1] 赵德化[2] 梅其炳[2] 孙本韬[3]
机构地区:[1]第四军医大学基础部病理生理学教研室,西安710033 [2]第四军医大学基础部药理学教研室,西安710033 [3]山西医学院电镜室
出 处:《第四军医大学学报》1998年第5期564-566,共3页Journal of the Fourth Military Medical University
摘 要:目的:探讨2,6-二甲基-4-(2-氯苯基)-1,4-二氢-3,5-吡啶二羧酸二甲酯(DCDDP)对野百合碱(MCT)引起肺动脉高压(PH)时大鼠血浆和肺组织匀浆中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量的影响.方法:在给MCT(60mg·kg-1,sc)前30min和后每日腹腔注射不同刘量(5,50,500μg·kg-1)DCDDP-次,用化学比色法测定SOD活性和MDA含量变化,用彩色图像分析仪观察肺小血管组织病理学的变化.结果;在注射MCT后4WK,大鼠静脉血浆和肺匀浆中SOD活性(106±45,317±59NU·L-1)明显低于对照组(155±28,505±47NU.L-1P分别为<0.05和<0.o1)、DCDDP能有效地阻止MCT引起的SOD活性下降,尤以中、低剂量组效果为佳(P分别为<0.05和<0.01).MCT组血浆和肺匀浆中MDA含量(15±5,59±14μmol·L-1)明显高于对照组(5.3±2.9,32±19μmol·L-1,P〈0.01),三种不同剂量的DCDDP都能够显著对抗肺匀浆中MCT引起的MDA含量升高(P<0.01).结论:DCDDP对MCT引起大鼠PH时血浆和肺匀浆中SOD活性的下降和肺匀浆中MDA含量的升高有明显的抑制作用,并能减轻MCT引起的淋巴细胞浸润现象,抑制肺小动脉管壁的变化,且以中、小剂量效果明显.这可能与其升高肺组织中NO含量有关,提示DCDDP对防治肺动脉?Aim: To investigate the effect of dimethyl 4-(2-chlorophenyl )-1, 4-dihydro-2, 6-dimethyl-3, 5-pyridinedi-carboxylate (DCDDP), a dihydropyridine calcium antagonist, on superoxide dismutase (SOD) activity and malondialdehyde (MDA ) concentration in plasma and pulmonaryhomogenate in rat with pulmonary hypertension (PH ),mold of PH was Induced by a singal subcutaneous injectionof monocrotaline (MCT, 60 mg·kg-1). Methods: Threedoses (5, 50, 500 μp·kg-1 ) of DCDDP were injected by ip30 min before and once daily after MCT injection. Thechanges in SOD activity and MDA concentration were me-asured by colorimetric analysis, histopathologic changes inlung and pulmonary small arteries were observed withcolour image analysis system. Results: Four weeks after injection of MCT, the SOD activity in plasma (106 ± 45 NU·L-1 ) and pulmonary homogenate (317 ± 59 NU· L-1 ) weresignificant lower than that of control (155 ± 28, 505 ± 47 re-spectively P < 0. 05 or P < 0. 01 ). The MDA content inplasma (15±μmol· L-1 ) and pulmonary homogenate (59± 14 μmol·L-1 ) in MCT group were significant higherthan that of control (5. 3± 2. 9, 32 ± 19 μmol·L-1, P〈0' 05 or P< 0. 01 ). DCDDP can effectively inhibit the de-crease in SOD activity, especially in middle dose (147 ±17,421 ± 54 NU·L-1) and low dose (173±29,406±73NU·L-1 P< 0. 05,or P< 0.01 )and prevent the MDA content increased by MCT in pulmonary homogenate (P < 0.01 ).Conclusion: DCDDP can significantly inhibit the SOD activi-ty lowered and prevent the MDA content elevated by MCTin plasma and pulmonary homogenate. These may be relat-ed to its mechanism of NO elevated in Pulmonary ho-mogenate and treatment PH.
分 类 号:R543.2[医药卫生—心血管疾病] R972[医药卫生—内科学]
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