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Inhaled Nitric Oxide Does Not Change Transpulmonary Angiotensin II Formation in Patients With Acute Respiratory Distress Syndrome FREE TO VIEW

Maieli Wenz; Regina Steinau; Herwig Gerlach; Margareta Lange; Gabriele Kaczmarczyk
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From the Clinic of Anesthesiology and Operative Intensive Medicine, Virchow-Klinikum der Humboldt-Universität zu Berlin, Germany

1997 by the American College of Chest Physicians

Chest. 1997;112(2):478-483. doi:10.1378/chest.112.2.478
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Study objective: To investigate the effect of short-term inhalation of nitric oxide (NO) on transpulmonary angiotensin II formation in patients with severe ARDS.

Design: Prospective, clinical study.

Setting: Anesthesiology ICU of a university hospital.

Patients: Ten ARDS patients who responded to inhalation of 100 ppm NO by decreasing their pulmonary vascular resistance (PVR) by at least 20 dyne·s·cm−5 were included in the study.

Interventions and measurements: In addition to standard treatment, the patients inhaled 0,1, and 100 ppm NO in 20-min intervals. Fraction of inspired oxygen was 1.0. Hemodynamics were measured and recorded online. Mixed venous (pulmonary arterial catheter) and arterial (arterial catheter) blood samples were taken simultaneously for hormonal analyses at the end of each inhalation period.

Results: Pulmonary arterial pressure decreased from 33±2 mm Hg (0 ppm NO, mean±SEM) to 29±2 mm Hg (1 ppm NO, p<0.05), and to 27±2 mm Hg (100 ppm NO, p<0.05, vs 0 ppm). PVR decreased from 298±56 (0 ppm NO) to 243±45 dyne·s·cm−5 (1 ppm NO, not significant [NS]), and to 197±34 dyne·s·cm−5 (100 ppm NO, p<0.05, vs 0 ppm). Arterial oxygen pressure increased from 174±23 mm Hg (0 ppm NO) to 205±26 mm Hg (1 ppm NO, NS), and to 245±25 mm Hg (100 ppm NO, p <0.05, vs 0 ppm). Mean plasma angiotensin II concentrations were 85±20 (arterial) and 57±13 pg/mL (mixed venous) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean transpulmonary plasma angiotensin II concentration gradient (=difference between arterial and mixed venous blood values) was 28±8 pg/mL (range, 0 to 69) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean transpulmonary angiotensin II formation (transpulmonary angiotensin II gradient multiplied with the cardiac index) was 117±39 ng/min/m2 (range, 0 to 414) during 0 ppm NO and did not change during inhalation of 1 and 100 ppm NO. Mean arterial plasma cyclic guanosine monophosphate concentration was 11±2 pmol/mL (0 ppm NO), did not change during 1 ppm NO, and increased to 58±8 pmol/mL (100 ppm NO, p<0.05). Arterial plasma concentrations of aldosterone (142±47 pg/mL), atrial natriuretic peptide (114±34 pg/mL), angiotensin-converting enzyme (30±5 U/L), and plasma renin activity (94±26 ng/mL/h of angiotensin I) did not change.

Conclusion: The decrease of PVR by short-term NO inhalation in ARDS patients was not accompanied by changes in transpulmonary angiotensin II formation. Our results do not support any relationship between transpulmonary angiotensin II formation and the decrease in PVR induced by inhaled NO.




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