The role of endothelin-1 as a mediator of the pressure response after air embolism in blood perfused lungs
The role of endothelin-1 as a mediator of the pressure response after air embolism in blood perfused lungs
复制标题
内皮素-1作为血液灌注肺部空气栓塞后压力反应介质的作用
DOI：
10.1007/s001340050622
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发表时间：
1998
影响因子：
38.9
通讯作者：
H. Neuhof
中科院分区：
文献类型：
--
作者：
J. Schmeck;T. Koch;A. Heller;K. Ackern;B. Patt;H. Neuhof
目的：众所周知，肺栓塞与肺血管阻力增加有关。由于栓塞期间肺血管反应的机制尚不清楚，本研究的目的是研究内皮素-1 （ET-1）和血栓素A2 （TXA2）作为栓塞后肺动脉压（PAP）升高的介质的潜在参与，使用选择性ETA受体拮抗剂LU135252[1]、ETB受体拮抗剂BQ788[2]和cyc - cloxgenase抑制剂双氯芬酸。设计：兔前瞻性实验研究。地点：大学教学医院实验室。实验对象：36只雌雄不限的成年兔子。干预措施：实验在36只分离和通气的兔肺中进行，肺内灌注含有10%自体血液的缓冲溶液。肺动脉内注射0.75 ml空气诱导栓塞。测量和结果：连续记录PAP和肺重量，反映水肿的形成。间歇抽取灌注液样品，测定TXA2和ET-1浓度。空气注入导致PAP在2.5分钟内立即增加22.8±1.4 mm Hg（对照组，n=6），与此同时，TXA2的生成也增强了。观察期间无相关水肿形成。ETA受体拮抗剂LU135 252预处理可显著降低空气栓塞后的压力反应（p<0.001），而ETB受体拮抗剂BQ788 （n=6）无明显作用。双氯芬酸组（n=6）在栓塞后2.5 min未改变PAP升高，但在进一步观察期间显著降低了压力反应（p<0.001）。lu135252与双氯芬酸联合应用（n=6）也显著降低了总观察期内PAP的增加，从2.5 min减少（p < 0.001）。结论：空气栓塞后急性压力反应主要通过ET-1介导，其机制与ETA受体相关。TXA2似乎维持这种反应的时间更长。
Objective: It is well known that lung embolism is associated with an increase in pulmonary vascular resistance. Since the mechanisms of pulmonary vascular reactions during embolism are still unclear, the aim of this study was to investigate the potential involvement of endothelin-1 (ET-1) and thromboxane A2 (TXA2) as mediators of the pulmonary artery pressure (PAP) increase after embolism using the selective ETA receptor antagonist LU135252 [1], the ETB receptor antagonist BQ788 [2], and the cy-clooxygenase inhibitor diclofenac.Design: Prospective experimental study in rabbits.Setting: Experimental laboratory in a university teaching hospital.Subjects: 36 adult rabbits of either sex.Interventions: The experiments were performed in 36 isolated and ventilated rabbit lungs which were perfused with a buffer solution containing 10 % of autologous blood. Embolism was induced by the injection of 0.75 ml air into the pulmonary artery.Measurements and results: PAP and lung weight, reflecting edema formation, were continuously recorded. Perfusate samples were drawn intermittently to determine TXA2 and ET-1 concentrations. Air injection resulted in an immediate increase in PAP up to 22.8 ± 1.4 mm Hg at 2.5 min (control, n=6), which was parallelled by an enhanced generation of TXA2. No relevant edema formation occurred during the observation period. Pretreatment with the ETA receptor antagonist LU135 252 significantly reduced the pressure reaction after air embolism (p<0.001) whereas the ETB receptor antagonist BQ788 (n=6) was without marked effects. The administration of diclofenac (n=6) did not alter the PAP increase 2.5 min after embolism, but significantly reduced the pressure reaction during the further observation period (p<0.001). The application of LU135 252 and diclofenac together (n=6) also significantly reduced the PAP increase from 2.5 min during the total observation period (p < 0.001).Conclusions: The acute pressure reaction after air embolism is mainly mediated via ET-1 by an ETA receptor related mechanism. TXA2 seems to maintain this reaction for a longer time.
DOI：
10.1152/ajplung.1995.269.5.l690
发表时间：
1995-11-01
影响因子：
4.9
作者：
DICARLO, VS;CHEN, SJ;OPARIL, S
通讯作者：
OPARIL, S
对绵羊进行连续空气栓塞会导致持续性肺动脉高压和肺血管反应性增加。
DOI：
--
发表时间：
1988
期刊：
The American journal of pathology
影响因子：
--
作者：
Perkett,EA;Brigham,KL;Meyrick,B
通讯作者：
Meyrick,B