Exhaled Oral and Nasal Nitric Oxide during L-Arginine Infusion in Preeclampsia
Objective: To determine the effects of the nitric oxide (NO) precursor L-arginine on the airway NO concentration in patients with preeclampsia. Methods: NO was measured by a noninvasive chemiluminescence technique in air sampled directly from nasal and oral cavities during expiration before and duri...
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Published in | Gynecologic and obstetric investigation Vol. 46; no. 4; pp. 232 - 237 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Basel, Switzerland
Karger
01.01.1998
S. Karger AG |
Subjects | |
Online Access | Get full text |
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Summary: | Objective: To determine the effects of the nitric oxide (NO) precursor L-arginine on the airway NO concentration in patients with preeclampsia. Methods: NO was measured by a noninvasive chemiluminescence technique in air sampled directly from nasal and oral cavities during expiration before and during L-arginine infusion in 9 preeclamptic and 10 control pregnancies. Maternal blood pressure and heart rate were simultaneously recorded, and blood was sampled for analyses of cyclic guanosine monophosphate (cGMP) and nitrate. Results: Basal nasal and orally exhaled NO and the increment in nasal NO concentration during L-arginine infusion were similar in both groups. Basal plasma and platelet cGMP concentrations were similar in both groups. Following L-arginine infusion, plasma cGMP levels were significantly higher in preeclamptics (p < 0.01), while platelet cGMP was unaffected in both groups. Basal plasma nitrate was significantly higher in preeclamptics (p < 0.01), and this difference was not altered following infusion. Blood pressure and heart rate remained unaffected by the procedure in both groups. Conclusions: Blood pressure did not decrease in the preeclamptics following L-arginine infusion, despite a significant increase in nasal NO sampled during breathhold and a concomitant increase in plasma cGMP, possibly reflecting an endogenous NO production. These results do not support the idea of a generalized decrease in NO production being a major cause of hypertension in preeclampsia. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0378-7346 1423-002X |
DOI: | 10.1159/000010040 |