1Department of Pediatric Intensive Care, Emma Children's Hospital/Academic Medical Center, Amsterdam, the Netherlands. 2Departments of Respiratory Medicine and Experimental Immunology, Academic Medical Center, Amsterdam, the Netherlands. 3Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. 4Department of Pathology, Academic Medical Center, Amsterdam, the Netherlands.
Pediatr Crit Care Med. 2013 Nov;14(9):e438-41. doi: 10.1097/PCC.0b013e3182a55735.
Angiotensin-converting enzyme and its effector peptide angiotensin II have been implicated in the pathogenesis of acute respiratory distress syndrome. Recently, angiotensin-converting enzyme 2 was identified as the counter-regulatory enzyme of angiotensin-converting enzyme that converts angiotensin II into angiotensin-(1-7). The aim of this study was to determine pulmonary angiotensin-converting enzyme and angiotensin-converting enzyme 2 activity in patients with acute respiratory distress syndrome.
Prospective observational pilot study.
A PICU of a university hospital.
Fourteen patients admitted, requiring mechanical ventilation for respiratory syncytial virus lower respiratory tract infection.
None.
Two groups of patients were distinguished at admission: a group fulfilling the criteria for acute respiratory distress syndrome and a non-acute respiratory distress syndrome group. Angiotensin-converting enzyme and angiotensin-converting enzyme 2 activity were measured in bronchoalveolar lavage fluid. Patients with acute respiratory distress syndrome had increased angiotensin-converting enzyme activity and decreased angiotensin-converting enzyme 2 activity (p < 0.001) compared with the control group.
It is shown for the first time that in acute respiratory distress syndrome, enhanced angiotensin-converting enzyme activity is paralleled by a reduced angiotensin-converting enzyme 2 activity, similar to that found in an experimental rat model of acute respiratory distress syndrome. The reduced angiotensin-converting enzyme 2 activity may be counteracted by restoring angiotensin-(1-7) level, thereby offering a novel treatment modality for this syndrome.
血管紧张素转换酶及其效应肽血管紧张素 II 被认为与急性呼吸窘迫综合征的发病机制有关。最近,血管紧张素转换酶 2 被鉴定为血管紧张素转换酶的拮抗酶,可将血管紧张素 II 转化为血管紧张素-(1-7)。本研究旨在确定急性呼吸窘迫综合征患者的肺血管紧张素转换酶和血管紧张素转换酶 2 活性。
前瞻性观察性初步研究。
大学医院的 PICU。
14 名因呼吸道合胞病毒下呼吸道感染而需要机械通气的患者。
无。
入院时区分出两组患者:一组符合急性呼吸窘迫综合征标准,一组不符合急性呼吸窘迫综合征标准。测量支气管肺泡灌洗液中的血管紧张素转换酶和血管紧张素转换酶 2 活性。与对照组相比,急性呼吸窘迫综合征患者的血管紧张素转换酶活性增加,血管紧张素转换酶 2 活性降低(p<0.001)。
这是首次表明,在急性呼吸窘迫综合征中,增强的血管紧张素转换酶活性伴随着血管紧张素转换酶 2 活性的降低,类似于在急性呼吸窘迫综合征的实验大鼠模型中发现的情况。通过恢复血管紧张素-(1-7)水平可以抵消血管紧张素转换酶 2 活性的降低,从而为这种综合征提供一种新的治疗方法。