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.
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.
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.
The authors have disclosed that they do not have any potential conflicts of interest.
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