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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。
In order to explore the role of calmodulin (CaM) in the pathogenesis of chronic hypoxic pulmonary hypertension, 40 Wistar rats were randomly divided into four groups. Group Ⅰ was normal control group and did not receive any treatment. Groups Ⅱ, Ⅲ and Ⅳ were divided into experimental group and hypoxia for 1, 2, and 3 weeks respectively. Ca2 + content and CaM activity in lung tissue of four groups were determined by flame atomic absorption spectrophotometry and phosphodiesterase assay. The results showed that both hypoxia and hypoxia could induce an increase in mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance (PVR) in rats and a decrease in cardiac output (CO); Ca2 + Compared with the normal control group, the CaM activity in the lung tissue of hypoxia 2 weeks and 3 weeks group was significantly different (P <0.05), but CaM activity in the 1 week hypoxia group was significantly higher than that in the normal control group (P <0.05), suggesting that Ca2 + -CaM system plays a role in the pathogenesis of hypoxic pulmonary hypertension in rats. Increased intracellular Ca2 + concentration may promote the migration of CaM from the cytoskeleton to the cytoplasm, which may be one of the reasons for the increased CaM activity in lung tissue of chronic hypoxia rats.