摘要
为探讨钙调素(CaM)在慢性缺氧性肺动脉高压发病中的作用,将40只Wistar大鼠随机分为四组,Ⅰ组为正常对照组,不接受任何处理。Ⅱ、Ⅲ、Ⅳ组为实验组,分别间断缺氧1、2、3周,而后采用火焰原子吸收分光光度法及磷酸二酯酶法测定四组大鼠肺组织Ca2+含量及CaM活性。结果显示:缺氧1、2、3周均能引起大鼠平均肺动脉压(mPAP)及肺血管阻力(PVR)增高,心输出量(CO)降低;缺氧大鼠肺组织Ca2+含量及CaM活性较正常对照组增高,其中缺氧2周及3周组大鼠肺组织CaM活性与正常对照组比较有显著性差异(P<0.05),但缺氧1周组大鼠CaM活性与正常对照组比较差异无统计学意义;肺组织Ca2+含量与CaM活性呈明显正相关(P<0.05),提示Ca2+-CaM系统在大鼠缺氧性肺动脉高压的发生中起一定作用。细胞内Ca2+浓度增高,可促使CaM由细胞骨架移行到细胞浆内,可能是慢性缺氧大鼠肺组织CaM活性增高的原因之一。
To investigate the effects of chronic hypoxia of calmodulin activity in rats, we divided 40 wistar rats into four major groups. One group acted as control. The other three groups were made hypoxic by placing them in an isobaric hypoxic chamber (O 2=10%) for 1, 2 and 3 weeks respectively. Calmodulin activity was measured by Phosphodiesterase method. The results showed that the mean pulmonary arterial presure and the pulmonary vascular resistance in rats were remarkably increased by chronic hypoxia. The total calcium levels and the calmodulin content in the lung tissue of rats were significantly elevated at 2 3 weeks of hypoxia exposure. However, the calmodulin content in the lung tissue of the rats exposed to hypo xia for 1 week also increased, but it was lower than those at 2 3 weeks of hypoxia exposure. Therefore, we conclude that Ca 2+ calmodulin system may play a central role in mediating hypoxai induced pulmonary hypertension.
出处
《华西医科大学学报》
CSCD
1997年第1期73-76,共4页
Journal of West China University of Medical Sciences
基金
四川省科委应用基础研究基金
关键词
缺氧性
肺性高血压
钙调素
Hypoxia Calmodulin Calcium Hypertension Pulmonary