慢性肺心病时血浆内皮素升高机制及其与肺动脉高压关系的研究

MECHANISMOFPLASMAENDOTHELIN┐1LEVELELEVATIONANDITSRELATIONWITHPULMONARYHYPERTENSIONINCHRONICCORPULMONALE

为了解慢性肺心病时血浆内皮素升高机制及其与肺动脉高压的关系，应用放射免疫法测定了２１例肺心病急性加重期患者的血浆内皮素－１（ＥＴ－１）水平并同步做了心导管检查。结果显示肺心病患者外周静脉血浆ＥＴ－１水平显著高于健康对照组，并且显著高于其自身的外周动脉和肺动脉血浆的ＥＴ－１水平。血浆ＥＴ－１水平与肺动脉平均压（ＰＡＰＭ），肺血管阻力指数（ＰＶＲＩ）呈显著正相关，而与动脉血氧分压（ＰａＯ２）呈显著负相关。机械通气后ＰａＯ２显著上升，血浆ＥＴ－１水平显著下降，ＰＡＰＭ与ＰＶＲＩ亦显著下降。提示缺氧导致血管内皮释放ＥＴ－１增多及肺部病变所致对ＥＴ－１清除代谢能力降低是引起肺心病加重期血浆ＥＴ－１增高的重要原因。血浆ＥＴ－１升高可导致肺动脉高压。积极改善缺氧，可明显降低血浆ＥＴ－１水平，改善肺心病的肺循环血流动力学状况。

Toexplorethemechanismofplasmaendothelin-1(ET-1)levelelevationanditsrelationwithpulmonaryhypertensioninchroniccorpulmonale,plasmaET-1levelwasmeasuredbyusingra-dioiM-munoassayin21casesofchroniccorpulmonalewithacuteexacerbationandcardiaccatheteriza-tionwasper-formedsimultaneously.Results:PeripheralvenousplasmaET-1levelofthepatientswassignificantlyhigherthanthatofcontrolsandalsohigherthanthatofperipheralarterialandpulmonaryarterialplasmaET-1levelofthepatientsthemselves.TheplasmaET-1levelofpatientshadasignificantnegativecorrela-tionwithPaO2andSaO2andpositivecorrelationwithmeanpulmonaryarterialpressure(PAPM)andpul-monaryvescularresistanceindex(PVRI).9ofthepatientsweretreatedwithmechani-calventilation.Afterventilation,PaO2wentupnotablyandplasmaET-1leveldecreasedremarkably;PAPMandPVRIalsoreducedsimultaneously.Conclusions:ThecausesofplasmaET-1levelelevationincorpulmonalemaybeasfolows,Firstly,pulmonaryalveolarhypoxiaincreasesthereleaseofET-1inlungs;Secondly,theabilityofthelungstocleanET-1decreasesbecauseofpulmonaryabnormality.HighlevelofplasmaET-1mayinducepulmonaryhypertension.ThelevelofplasmaET-1canbeloweredbycorrectinghypoxicstatusofthepatientsandtheresultingimprovementofpulmonaryhemodynamics.