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[哮喘豚鼠血管紧张素系统活性变化及皮质类固醇对其的影响]

[Change of angiotensin system activity and the effects of corticosteroid on it in asthmatic guinea pigs].

作者信息

Qian X, Lin Y, Sun M

机构信息

Department of Respiratory Disease, PUMC Hospital, CAMS and PUMC, Beijing 100730, China.

出版信息

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2000 Dec;22(6):577-9.

Abstract

OBJECTIVE

To investigate the role of angiotensin system(ATs) and effect of corticosteroid on ATs activity at the onset of asthma.

METHODS

After establishing asthmatic model of guinea pig by intraperitoneal injection with ovalbumin to sensitize and inhalation with the same sensitizer 3 weeks later to induce asthma attack, the levels of angiotensin(AT) I and AT II and the activity of angiotensin converting enzyme(ACE) were measured respectively in extractive fluid of chopped lung tissue, bronchial alveolar lavage fluid (BALF) and plasma (ACE activity in serum) in three groups of experimental guinea pigs including asthmatic group, control group and corticosteroid group.

RESULTS

In the chopped lung tissue and BALF, the AT I, AT II levels and the ACE activity in the asthmatic group were significantly higher than that in the control group(P < 0.01), however, they did not differ significantly each other in plasma in three groups(P > 0.05). In corticosteroid group, the levels of AT I, AT II and ACE activity were significantly decreased in the BALF compared with that in the asthmatic group(P < 0.01).

CONCLUSION

The results suggest that the lung tissue may have a local angiotensin system that may be activated and play a role in asthma attack, and the inhibition of ATs activity may be one of the mechanisms in the effects of inhaled corticosteroid on prevention and control of asthma.

摘要

目的

探讨血管紧张素系统(ATs)在哮喘发作时的作用及皮质类固醇对ATs活性的影响。

方法

通过腹腔注射卵清蛋白致敏豚鼠,3周后用同一致敏原雾化吸入诱发哮喘发作,建立豚鼠哮喘模型。分别测定哮喘组、对照组和皮质类固醇组三组实验豚鼠肺组织匀浆、支气管肺泡灌洗液(BALF)及血浆(血清中ACE活性)中血管紧张素(AT)Ⅰ、ATⅡ水平及血管紧张素转换酶(ACE)活性。

结果

在肺组织匀浆和BALF中,哮喘组ATⅠ、ATⅡ水平及ACE活性均显著高于对照组(P<0.01),但三组血浆中上述指标差异无统计学意义(P>0.05)。与哮喘组相比,皮质类固醇组BALF中ATⅠ、ATⅡ水平及ACE活性显著降低(P<0.01)。

结论

结果提示肺组织可能存在局部血管紧张素系统,该系统可能被激活并在哮喘发作中起作用,抑制ATs活性可能是吸入性皮质类固醇防治哮喘作用机制之一。

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