摘要
目的通过研究肺通气功能障碍与血浆血管紧张素Ⅱ（ＡＴⅡ）、肾素活性（ＰＲＡ）和醛固酮（Ａｌｄ）水平的关系，探索慢性阻塞性肺疾病（ＣＯＰＤ）导致肺动脉高压的早期发病机理。方法测定小气道功能、第一秒用力呼气容积（ＦＥＶ１）和肺容量正常的高龄非吸烟健康人１２例和缓解期慢性支气管炎伴或不伴有肺气肿２３例患者的坐位血浆ＡＴⅡ、ＰＲＡ和Ａｌｄ水平。结果小气道功能障碍和ＦＥＶ１障碍对ＰＲＡ、ＡＴⅡ和Ａｌｄ的代谢有显著的影响。小气道功能障碍而ＦＥＶ１正常的患者，ＡＴⅡ水平即有显著升高。气道阻塞导致中度肺气肿时ＡＴⅡ升高最明显，ＰＲＡ也有显著升高。结论结果表明慢性支气管炎导致的早期肺通气功能障碍即可影响ＰＲＡ、ＡＴⅡ的代谢，使ＡＴⅡ水平升高，这些变化与动脉血氧分压（ＰａＯ２）水平无关，是否为ＣＯＰＤ早期肺动脉高压的发病机理之一，值得进一步研究。
ObjectiveRAASwasdeterminedtoinvestigatetherelationshipbetweentheirchangesandthedys-functionofpulmonaryventilationforevaluatingthepathogenesisofearlypulmonaryhyper-tensioninchronicbronchitiswithorwithoutemphysema.MethodsAngiotensinⅡ(ATⅡ),plasmareninactivity(PRA)andaldos-terone(Ald)weredeterminedat8:00AMinsitingpositionfor30minutesin12heathynonsmokers,50～60yearsold,withnormalfunctionsofsmalairway,normalFEV1andlungvolumes,andin23patientswithchronicbronchi-tiswithorwithoutemphysema.ResultsAlpatientswithchronicbronchitisshoweddysfunctionofsmalairwaywithorwithoutabnormalitiesofFEV1andlungvolumes.Inhealthycontrolgroup,theplasmaPRA,ATⅡandAldlevelswere0.22±0.12μg·L-1·h-1(x±sx),52±7ng/Land315±26pmol/Lrespectivelycomparingwiththoselevelsof0.43±0.11μg·L-1·h-1,197±32ng/Land388±59pmol/Linagedpatientswithchronicbronchitis.ItwasfoundthatdysfunctionofsmalairwayalonecouldcauseremarkableelevationofPRAandATⅡlevels.Inpa-tientswithmildpulmonaryemphysema,thelevelsofPRAandATⅡweresignificantlyincreased.ThemoderatepulmonaryemphysemainducedgreatlyincreaseofPRA,ATⅡandAldlevels.Inpatientswithseverepulmonaryemphysema,however,theplasmalevelsofPRAandATⅡweresignificantlyatenuatedfromthelevelsinmoderatepulmonaryemphysemawhileAldlevelwasstilgetinghigher.TherewerenoevidencetoindicatetherelationshipbetwenthechangesofRAASandhypoxemia.ConclusionTheelevationofATⅡandPRAmightpartlybethepathogenesisofearlypulmonaryhypertensioninCOPD.
出处
《中华结核和呼吸杂志》
CAS
CSCD
北大核心
1996年第2期84-87,共4页
Chinese Journal of Tuberculosis and Respiratory Diseases
基金
国家自然科学基金
