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成人呼吸窘迫综合征患者血清样本中的中性内肽酶。与血管紧张素转换酶的比较。

Neutral endopeptidase in serum samples from patients with adult respiratory distress syndrome. Comparison with angiotensin-converting enzyme.

作者信息

Johnson A R, Coalson J J, Ashton J, Larumbide M, Erdös E G

出版信息

Am Rev Respir Dis. 1985 Dec;132(6):1262-7. doi: 10.1164/arrd.1985.132.6.1262.

Abstract

The activities of 2 peptidases, angiotensin-I converting enzyme (ACE) and neutral metalloendopeptidase (NEP), were measured in serum from patients with adult respiratory distress syndrome (ARDS). As noted by others, we found that the specific activity of serum ACE was reduced in patients with severe alveolocapillary damage caused by ARDS. In addition, patients who were severely ill with chronic obstructive lung disease had lower serum ACE than did normal ambulatory control subjects. Patients with cardiogenic pulmonary edema, however, had no consistent loss of the enzyme. The most striking changes occurred in the serum levels of NEP. Whereas the specific activity of this enzyme was very low in the normal subjects, it was elevated as much as 50- to 60-fold in serum samples from patients with ARDS. Serum from patients with cardiogenic pulmonary edema had high levels of NEP, and it was elevated also in a subset of patients with chronic obstructive lung disease. On the assumption that patients with ARDS sustain significant damage at the alveolar-capillary level, these changes in ACE and NEP could signal endothelial damage; ACE loss could result from direct injury to the vascular lumen, and NEP from subendothelial tissues could enter the bloodstream through damaged endothelium. Alternatively, NEP might be released from leukocytes sequestered in the lung and leak into the bloodstream.

摘要

在成人呼吸窘迫综合征(ARDS)患者的血清中检测了两种肽酶——血管紧张素I转换酶(ACE)和中性金属内肽酶(NEP)的活性。正如其他人所指出的,我们发现ARDS导致严重肺泡毛细血管损伤的患者血清ACE的比活性降低。此外,患有慢性阻塞性肺疾病的重症患者血清ACE低于正常活动对照受试者。然而,心源性肺水肿患者并未出现该酶的持续丧失。最显著的变化发生在NEP的血清水平上。该酶在正常受试者中的比活性非常低,而在ARDS患者的血清样本中却升高了50至60倍。心源性肺水肿患者的血清NEP水平较高,在一部分慢性阻塞性肺疾病患者中也有所升高。假设ARDS患者在肺泡-毛细血管水平遭受了严重损伤,ACE和NEP的这些变化可能表明内皮损伤;ACE的丧失可能是由于血管腔直接受损,而来自内皮下组织的NEP可能通过受损的内皮进入血液。或者,NEP可能从滞留在肺部的白细胞中释放出来并泄漏到血液中。

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