Abstract: Poster Presentations |

Cardiac Muscle Mass and Wall Thickness in Fetal Lambs with Pulmonary Hypertension FREE TO VIEW

Frederick C. Morin, MD; Vicki L. Mahan, MD*
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Women and Children’s Hospital of Buffalo, Buffalo, NY


Chest. 2004;126(4_MeetingAbstracts):882S-b-883S. doi:10.1378/chest.126.4_MeetingAbstracts.882S-b
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PURPOSE:  In our fetal lamb model of PPHN, created by prenatal ligation of the ductus arteriosus, we found that endothelial NO gene expression is attenuated and that this may contribute to abnormal vasoreactivity and muscularization of the pulmonary circulation in fetal hypertension. This study characterizes changes in the cardiac muscle mass and wall thickness and pulmonary physiology in this model.

METHODS:  Six experimental fetuses who had their ductus arteriosus ligated, three control fetuses who had sham ligation of the ductus arteriosus before delivery, and six control fetuses who had no prenatal surgery were delivered by cesarean section. Each was instrumented to measure pulmonary artery pressure and systemic arterial pressure and pulmonary blood flows. Each newborn lamb was ventilated with room air during the first 45 minutes after delivery and then with decreasing amounts of inspired oxygen.

RESULTS:  Pulmonary arterial pressure decreased significantly when ventilation was begun in the control lambs but not in the study animals. Pulmonary arterial pressure and total pulmonary resistance were higher, and pulmonary blood flow was lower in the ligated lambs. Similarly, a group of lambs 133 to 142 days gestation, 11 control and 11 ligated for 4 to 17 days were used for heart measurement comparisons. Right ventricular wall thickness was increased in the lambs that had their ductus arteriosus ligated. Left ventricle, right ventricle, and septal weights were also higher in the ligated animals.

CONCLUSION:  These pathologic and physiologic changes are most likely due to the intra-uterine development of pulmonary hypertension.

CLINICAL IMPLICATIONS:  Intra-uterine pulmonary hypertension may result in pathologic and physiologic changes in neonatal myocardium with subsequent poor outcomes. Prenatal treatment and management of pulmonary hypertension may improve outcome of this high risk population of patients.

DISCLOSURE:  V.L. Mahan, None.

Wednesday, October 27, 2004

12:30 PM- 2:00 PM




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