摘要
目的 :观察白藜芦醇苷对慢性常压低氧性肺动脉高压 (HPH)大鼠肺血管构型重建的影响并探讨可能的机理。方法 :2 9只健康SD大鼠随机分为正常对照组、单纯低氧组和低氧加白藜芦醇苷 (PD)组。各组内按照肺小血管外径分为I组 (30 μm - 1 0 0 μm)和II组 (1 0 1 μm - 2 0 0 μm)。右心导管法检测大鼠肺动脉压力 (mPAP)、微量滴定法检测血浆和肺匀浆中磷脂酶A2 (PLA2 )活性、光镜下观察肺小血管中膜厚度 (MT % )和中膜面积 (MA % )的变化。结果 :低氧 3周后大鼠mPAP、血浆及肺匀浆中PLA2 活性、肺小血管MA %、I组MT %显著高于对照组 ,II组MT %无显著性改变。低氧加PD预处理后上述改变明显轻于单纯低氧组。结论 :PD可有效防治慢性常压低氧性大鼠肺动脉压力的升高 。
AIM: To study the relationship between the activity of phospholipase A 2 (PLA 2) and pulmonary structural remodeling with the model of chronic isobaric hypoxic pulmonary hypertension. METHODS: 29 healthy Sprague-Dawley rats were randomly divided into normal control group, chronic hypoxic group and hypoxia plus Polidatin (PD) group. By diameter, the arteries were divided into two groups: arteries of group I (30 μm-100 μm) and group II (101 μm-200 μm). The mean pulmonary arterial pressure (mPAP) was measured by inserting a microcatheter into the pulmonary artery. The PLA 2 activity was measured with modified microtitrimetic method. The pulmonary tissue and arterioles morphology changes were examined under light microscope. RESULTS: It was found that after 21 days hypoxia, the mean pulmonary arterial pressure (mPAP), the PLA 2 activity in blood and lung homogenate increased significantly. The media thickness of group I arteries increased (P<0.01) while that of group II arteries had no significant changes. The ratio of media area and adventitia of both groups was raised. Under light microscope, it was observed that pulmonary vascular endothelium proliferated, media became thickening and adventitia matrix increased. Pretreatment with PD could attenuate the changes mentioned above. CONCLUSION:PLA 2 plays an important inducing role through promotion of the pulmonary vascular structural remodeling in the formation of chronic hypoxic pulmonary hypertension.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2002年第8期935-937,I002,共4页
Chinese Journal of Pathophysiology
基金
广东省科委自然科学基金资助项目 (No .960 761 )
