李筱玥，蔡秋瑾，张　欢，刘瑞欣，纪巧荣，周　振，张　伟

(青海大学医学院，西宁 810001)

急性低氧过程中内源性肾上腺素对麻醉大鼠低氧性肺水肿的保护机制※

李筱玥，蔡秋瑾，张欢，刘瑞欣，纪巧荣，周振，张伟*

(青海大学医学院，西宁 810001)

摘要目的探讨急性低氧过程中内源性肾上腺素对麻醉大鼠低氧性肺水肿的保护机制。方法将SD大鼠随机分为对照组、肾上腺切除组、低氧对照组和低氧肾上腺切除组。采用PowerLab生物信号采集系统分别在常氧(20%O2，80%N2)、低氧(15%O2，85%N2)条件下实时、动态监测系统平均动脉压(mean artery pressure，MAP)、肺动脉压(pulmonary artery pressure，PAP)、左心房压(left arterial pressure，LAP)、中心静脉压(central venous pressure，CVP)、气道压力(airway pressure，Paw)、升主动脉血流量(ascending aorta blood flow，ABF)和心率(heart rate，HR)，观察切除肾上腺后急性低氧对麻醉大鼠血流动力学的指标变化。结果常氧下肾上腺切除组的MAP、PAP、HR、ABF无明显变化。急性低氧过程中，对照组与肾上腺切除组的MAP、ABF、HR和体循环阻力(Toll resistance，TPR)均降低，PAP均增高(P<0.05)，差异有显著性；肾上腺切除组的肺循环阻力(Pulmonary vascular resistance，PVR)升高(P<0.05)；两组的LAP和Paw无明显变化。低氧对照组与对照组相比，则低氧对照组的MAP、ABF、TPR明显降低，PAP增高，差异有显著性。结论急性低氧刺激会使大鼠TPR降低，双侧肾上腺切除后会使大鼠的TPR进一步降低，且PVR升高。急性低氧过程中，肾上腺所分泌的内源性肾上腺素能在一定程度上抑制PAP的增高，可能是阻止机体发生低氧性肺水肿的机制。

关键词急性低氧内源性肾上腺素麻醉大鼠肺水肿机制

通信作者李筱玥(1989～)，女，汉族，河北籍，青海大学医学院2012级科学班研究生.*：，教授，博士生导师，电话：0971-6109507.

※：国家自然科学基金资助(No.81160012)，教育部新世纪优秀人才项目(No.NCET-12-1022)，青海省自然科学基金项目(No.2012-Z-915Q)，青海大学医学院中青年科研基金团队项目(No.2013-KT-4).

中图分类号R363

文献标识码识码A

DOI：10.13452/j.cnki.jqmc.2015.02.002

AbstractObjectiveTo investigate the protective mechanism of endogenous epinephrine for hypoxic pulmonary edema in anesthesia during acute hypoxia in rats.Methods SD rats were randomly divided into four groups：control group，adrenalectomy group，hypoxia control group and hypoxia adrenalectomy group(n=7).Using Power Lab biological signal collecting system under normoxia(20%O2，80%N2)and hypoxia(15%O2，85%N2)at the same time to detect the real-timely monitoring mean artery pressure (MAP)，pulmonary artery pressure(PAP)，left atrial pressure(LAP)，central vein pressure(CVP)，airway pressure(Paw)，ascending aorta blood flow(ABF)，heart rate(HR)，respectively，and the index changes of acute hypoxia on hemodynamics in anesthetized rats were observed after excision of adrenal gland.Results MAP，PAP，HR andABF in adrenalectomy group had no obvious change.In the process of acute hypoxia，all of MAP，ABF，HR，toll resistance and TPR in the control group and adrenalectomy group were decreased，whereas the PAP increased and showed a significant difference(P<0.05).Pulmonary vascular resistance and the PVR in the adrenal gland resection group were increased(P<0.05)；the two groups′ LAP and Paw had no obvious change.The hypoxial group′s MAP，ABF，TPR were significantly decreased.PAP in Hypoxia control group was increased compared with the control group，but the difference was significant.Conclusion Acute hypoxiacancan decrease the TPR in rats and adrenalectomy may further decrease the TPR and lead PVR increase.It shows that in acute hypoxia process，endogenous adrenaline secreted by the adrenal can inhibit the increase of pulmonary artery pressure in a certain extent，may be a protective mechanism for hypoxic pulmonary edema.

KeywordsAcuteHypoxiaEndogenous epinephrineAnesthesiaPulmonary edema

收稿日期2015-02-06

THE PROTECTIVE MECHANISM OF ENDOGENOUS

EPINEHYRINE FOR ANESTHETIZED HYPOXIC PULMONARY

EDEMA DURING ACUTE HYPOXIA IN RATS

Li Xiaoyue，Cai Qiujin，Zhang Huan，Liu Ruixin，Ji Qiaorong，Zhou Zhen，Zhang Wei*

(Qinghai University Medical College，Xining，Qinghai 810001，China)

急性高原病中以高原肺水肿(high altitude pulmonary edema，HAPE)和高原脑水肿(high altitude cerebral edema，HACE)较为多见，其中HAPE 的发病率高、危害性大[1]，也是引起HACE的主要原因。HAPE是由于高原低压缺氧、寒冷、疲劳所诱发的以急性肺水肿为临床表现的一种严重危及生命的疾病[2]。因此对HAPE发病机制的研究具有重大意义。……