Pulmonary hemodynamics in neonatal lambs resuscitated with 21%, 50%, and 100% oxygen
The effect of resuscitation with varying levels of O2 on pulmonary hemodynamics at birth is not well known. We hypothesized that the decrease in pulmonary vascular resistance (PVR) and subsequent response to pulmonary vasoconstrictors and vasodilators will differ following resuscitation with 21%, 50...
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Published in | Pediatric research Vol. 62; no. 3; pp. 313 - 318 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Hagerstown, MD
Lippincott Williams & Wilkins
01.09.2007
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Subjects | |
Online Access | Get full text |
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Summary: | The effect of resuscitation with varying levels of O2 on pulmonary hemodynamics at birth is not well known. We hypothesized that the decrease in pulmonary vascular resistance (PVR) and subsequent response to pulmonary vasoconstrictors and vasodilators will differ following resuscitation with 21%, 50%, or 100% O2 for 30 min at birth in normal term lambs. Lambs at 141 d gestation were delivered by cesarean section and ventilated with 21% (21% Res; n=6), 50% (50% Res; n=6), or 100% 02 (100% Res; n=7) for 30 min followed by ventilation with 21% O2 in all three groups. A greater decrease in PVR was seen with 50% and 100% O2 ventilation than with 21% O2 (0.21 +/- 0.02, 0.21 +/- 0.02, and 0.34 +/- 0.05 mm Hg/mL/min/kg, respectively). Subsequent pulmonary vasoconstriction to hypoxia (10% O2) and the thromboxane,analog U46619 (0.5 and 1 mcirog/kg/min) was similar in all three groups. After inducing a stable elevation in PVR with U46619, impaired pulmonary vasodilation to inhaled NO (59 +/- 4, 65 +/- 4, and 74 +/- 5% of baseline PVR with 21, 50, and 100%Res, respectively) and acetylcholine infusion (67 +/- 8, 75 +/- 6, and 87 +/- 4% of baseline PVR with 21, 50, and 100%Res, respectively) and rebound pulmonary hypertension following their withdrawal were observed in the 100%Res group. We conclude that, while ventilation with 100% O2 at birth results in a greater initial decrease in PVR, subsequent pulmonary vasodilation to NO/acetylcholine is impaired. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0031-3998 1530-0447 |
DOI: | 10.1203/PDR.0b013e3180db29fe |