摘要
目的:研究慢性缺氧对大鼠肺动脉平滑肌细胞(PASMCs)胞内钙浓度([Ca2+]i)的影响及L-型钙通道和胞内钙库的作用,为缺氧性肺动脉高压(HPH)发病机制的进一步研究提供理论依据。方法:复制大鼠缺氧性肺动脉高压动物模型,利用Fura-2/AM钙离子成像方法测定PASMCs在不同钙离子浓度细胞外液及L-型钙通道阻滞剂n ifed ip ine和IP3R钙通道抑制剂肝素干预前后[Ca2+]i变化。结果:(1)缺氧+含钙外液组PASMCs[Ca2+]i显著高于对照+含钙外液组(P<0.05)。缺氧+含钙外液组PASMCs[Ca2+]i显著高于缺氧+无钙外液组(P<0.05)。(2)缺氧n ifed ip ine组PASMCs[Ca2+]i在加药前后无显著差异(P>0.05)。(3)缺氧未干预组与缺氧肝素组PASMCs[Ca2+]i无明显差异(P>0.05)。结论:慢性缺氧可使PASMCs的[Ca2+]i增加。慢性缺氧引起[Ca2+]i增加可能与细胞外钙内流有关,L-型钙通道和IP3R钙通道在调节[Ca2+]i的过程中可能不独立发挥作用。
AIM ： To study the effect of chronic hypoxia （CH） on the intracellular calcium （ [ Ca^2＋] i） in pulmonary artery smooth muscle cells （PASMCs） and the role of L- type calcium channel and calcium store. METHODS： The rat chronic hypoxia model was set up and intervene the PASMCs with normal PSS, calcium -free PSS, nifedipine, and heparine respectively. The resting [ Ca^2＋] i was determined with the Fura - 2/AM calcium imaging technique. RESULTS ： （1） The [Ca^2＋]i in CH group in normal PSS was higher than that in control group in normal PSS （P 〈0.05）. The [ Ca^2＋ ] i in CH group in normal PSS was higher than that in calcium - free PSS （ P 〈 0. 05 ）. （ 2 ） No obvious change of [ Ca^2＋ ] i before and after application of nifedipine in PASMCs of CH groups was observed. （ 3 ） No difference of [ Ca^2＋ ] i before and after application of heparine in PASMCs of CH groups was detected. CONCLUSION ： Chronic hypoxia increased the [ Ca^2＋] i in PASMCs. Chronic hypoxia induced increase in [ Ca^2＋ ] i may relate to the influx of extracellular calcium, but not due to the L- type calciunl channel or the IP3 R modulation only.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2006年第11期2138-2141,共4页
Chinese Journal of Pathophysiology
关键词
缺氧
肺动脉平滑肌细胞
钙
钙通道
L-型
Anoxia
Pulmonary artery smooth muscle cells
Calcium
Calcium channels, L - type
