摘要
目的探讨汉防己甲素（Ｔｅｔ）降低缺氧性肺动脉高压的可能机制。方法将Ｗｉｓｔａｒ大鼠３０只分为正常对照组（Ⅰ组）、缺氧性肺动脉高压模型组（Ⅱ组）及Ｔｅｔ处理组（Ⅲ组）。采用火焰原子吸收分光光度法及磷酸二脂酶（ＰＤＥ）法测定肺组织Ｃａ２＋含量及钙调素（ＣａＭ）活性。结果Ｔｅｔ能明显降低缺氧性肺动脉高压大鼠的平均肺动脉压（ｍＰＡＰ）及肺血管阻力（ＰＶＲ），Ⅲ组肺组织Ｃａ２＋含量（６２±１０μｍｏｌ·ｇ－１）及肺组织ＣａＭ活性（２０±４ｎｇ·ｍｇ－１）较Ⅱ组肺组织Ｃａ２＋含量（７４±１６μｍｏｌ·ｇ－１）及肺组织ＣａＭ活性（２７±６ｎｇ·ｍｇ－１）明显降低（Ｐ＜０．０５）。直线相关分析显示Ｔｅｔ处理大鼠肺组织Ｃａ２＋Ｐ含量与ｍＰＡＰ及ＰＶＲ呈直线相关。结论Ｔｅｔ降低缺氧性肺动脉高压的作用与血管平滑肌细胞内Ｃａ２＋浓度降低有关，这种作用可能是拮抗ＣａＭ活性的结果。
ObjectiveThemechanismthattetrandrine(Tet)reduceshypoxicpulmonaryhyperten-sionwasinves┐tigatedMethod30Wistarratsweredividedintonormalcontrolgroup,pulmonaryhy-pertensiongroupandtetran-drine-treatedgroup.Totalcaciumconteinsandcalmodulinactivityinlungtisueweremeasuredwithatomicab-sorptionspectrophotometryandphosphodiesterasemethod.ResultsTheresultsshowedthatTetcouldremarkablyreducethemeanpulmonaryarterypresureandpulmonaryvascularresistanceinratswithhypoxicpulmonaryhy-pertension,thecontentsofcalcium(62±10umol.g-1)andcalmodulin(20±4ng.mg-1)inthelungweresignficantlylowerinratsadminis-tratedwithTetthanthose(74±16umol·g-1,27±6ng·mg-1)ratswithhypoxicpulmonaryhyper-tension,andthecontentsofcalciumwererelatedwiththemeanpulmonaryarterypresureandpul-monaryvascularresistanceinthelungadministratedwithTet.ConclusionTherauesindicatedthemechanismthattetran-drineefectivelyreduceshypoxiapulmonaryhypertensionmaybeassociatedwithdecreasingintracelularcalciumconcentrationinvascularsmoothcels,andtheefectmaybearesultofanti-calmodulinactivity.
出处
《中华结核和呼吸杂志》
CAS
CSCD
北大核心
1996年第2期75-77,共3页
Chinese Journal of Tuberculosis and Respiratory Diseases
基金
四川省应用基础研究资助
