Cromakalim 阻断内皮素-1介导肺动脉高压的研究  

Cromakalim Inhibts Endothelin1 Induced Pulmonary Hypertension in Rats

作　　者：程德云 陈文彬 肖欣荣 

出　　处：《华西医科大学学报》1998年第1期79-81,共3页Journal of West China University of Medical Sciences

摘　　要：内皮素－１（ＥＴ－１）和钾通道在肺动脉高压的发病中起重要作用。为了解ＡＴＰ敏感性钾通道开放剂对ＥＴ－１收缩肺血管效应的影响，对１０只Ｗｉｓｔａｒ大鼠预先采用肺动脉内注入ＥＴ－１（１．５μｇ／ｋｇ），形成肺动脉高压，然后采用ＡＴＰ敏感性钾通道开放剂Ｃｒｏｍａｋａｌｉｍ（１５０μｇ／ｋｇ）注入，记录注药前，注射ＥＴ－１后，以及使用Ｃｒｏｍａｋａｌｉｍ后１、５、１０分钟的大鼠肺血流动力学指标。结果：大鼠注入ＥＴ－１后，其ｍＰＡＰ升至３．３２±０．４９ｋＰａ，明显高于注射前的２．３６±０．２４ｋＰａ；应用Ｃｒｏｍａｋａｌｉｍ可明显降低ＥＴ－１导致的大鼠肺动脉高压，大鼠ｍＰＡＰ在注入１分钟时为２．５０±０．６２ｋＰａ，注入５分钟时为１．１４±０．１８ｋＰａ，注入１０分钟时为２．３３±０．５２ｋＰａ，同时伴有肺血管阻力降低。提示ＥＴ－１与钾通道之间存在相互作用，钾通道开放剂对ＥＴ－１收缩肺动脉的效应具有一定的抑制作用。There is evidence that endothelin1(ET1) and potassium channel may play an important role in the development of pulmonary hypertension.To evaluate the effect of ATPsensitive K+ channel opener on pulmonary hypertension induced by ET1,catheter was inserted into the pulmonary artery in ten male Wistar rats which had had pulmonary hypertension established by infusion of ET1 (1.5μg/kg), and then cromakalim were injected with a dose of 150μg/kg. The mean pulmonary arterial pressure (mPAP),cardiac output (CO) monitored before and after infusion of ET1,and 1 min,5 min,10 min after cromakalim injection,and pulmonary vascular resistance(PVR) were calculated.It was found that the mPAP was significantly increased,from 2.36±0.24 kPa to 3.32±0.49 kPa(P<0.01),and PVR also increased,by infusion of ET1.After cromakalim injection,mPAP were decreased to 2.50±0.62 kPa in 1 min,1.14±0.18 kPa in 5 min and 2.33±0.52 kpa in 10 min,PVR decreased significantly.It is suggested that there is interaction between ET1 and potassium Channel,and Cromakalim decreases mPAP in part by inhibiting the response of pulmonary artery to ET1.

关 键 词：内皮素-1 钾通道 CROMAKALIM 肺动脉高压 

分 类 号：R543.2[医药卫生—心血管疾病] R972[医药卫生—内科学]