0
Articles |

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

Maieli Wenz; Regina Steinau; Herwig Gerlach; Margareta Lange; Gabriele Kaczmarczyk
Author and Funding Information

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
Text Size: A A A
Published online

Abstract

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.


Sign In to Access Full Content

MEMBER & INDIVIDUAL SUBSCRIBER

Want Access?

NEW TO CHEST?

Become a CHEST member and receive a FREE subscription as a benefit of membership.

Individuals can purchase this article on ScienceDirect.

Individuals can purchase a subscription to the journal.

Individuals can purchase a subscription to the journal or buy individual articles.

Learn more about membership or Purchase a Full Subscription.

INSTITUTIONAL ACCESS

Institutional access is now available through ScienceDirect and can be purchased at myelsevier.com.

Sign In to Access Full Content

MEMBER & INDIVIDUAL SUBSCRIBER

Want Access?

NEW TO CHEST?

Become a CHEST member and receive a FREE subscription as a benefit of membership.

Individuals can purchase this article on ScienceDirect.

Individuals can purchase a subscription to the journal.

Individuals can purchase a subscription to the journal or buy individual articles.

Learn more about membership or Purchase a Full Subscription.

INSTITUTIONAL ACCESS

Institutional access is now available through ScienceDirect and can be purchased at myelsevier.com.

Figures

Tables

References

NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Sign In to Access Full Content

MEMBER & INDIVIDUAL SUBSCRIBER

Want Access?

NEW TO CHEST?

Become a CHEST member and receive a FREE subscription as a benefit of membership.

Individuals can purchase this article on ScienceDirect.

Individuals can purchase a subscription to the journal.

Individuals can purchase a subscription to the journal or buy individual articles.

Learn more about membership or Purchase a Full Subscription.

INSTITUTIONAL ACCESS

Institutional access is now available through ScienceDirect and can be purchased at myelsevier.com.

Related Content

Customize your page view by dragging & repositioning the boxes below.

Find Similar Articles
CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543