Hemodynamic, pulmonary vascular, and myocardial abnormalities secondary to pharmacologic constriction of the fetal ductus arteriosus. A possible mechanism for persistent pulmonary hypertension and transient tricuspid insufficiency in the newborn infant
| Autor: | D. L. Levin, L. J. Mills, A. G. Weinberg |
|---|---|
| Rok vydání: | 1979 |
| Předmět: |
Heart Defects
Congenital medicine.medical_specialty Hypertension Pulmonary Indomethacin Blood Pressure Constriction Pathologic Pulmonary Artery Inferior vena cava chemistry.chemical_compound Fetal Heart Physiology (medical) Ductus arteriosus Internal medicine Animals Humans Medicine Vascular Diseases cardiovascular diseases Prostaglandin E1 Lung Fetus Sheep Tricuspid valve business.industry Hemodynamics Ductus Arteriosus Tricuspid insufficiency medicine.disease Tricuspid Valve Insufficiency medicine.anatomical_structure Blood pressure medicine.vein chemistry Anesthesia embryonic structures cardiovascular system Vascular resistance Cardiology Blood Vessels Vascular Resistance Cardiology and Cardiovascular Medicine business |
| Zdroj: | Circulation. 60:360-364 |
| ISSN: | 1524-4539 0009-7322 |
| DOI: | 10.1161/01.cir.60.2.360 |
| Popis: | The prostaglandin synthetase inhibitor indomethacin was given orally or intravenously to pregnant ewes. This resulted in a significant rise in the fetal pulmonary-to-systemic arterial mean blood pressure difference across the ductus arteriosus, presumably secondary to constriction of the ductus arteriosus. In five experiments the pressure difference could be promptly but temporarily reversed by the administration of prostaglandin E1 (PGE1) into the fetal inferior vena cava. Fetal lungs from study and control animals were fixed by perfusion at measured pulmonary arterial mean blood pressure, and fifth-generation resistance vessels were studied. The medial width/external diameter ratio was significantly increased in the study vs the control lungs due to increased smooth muscle and decreased external diameter. In addition, study fetuses had acute degenerative myocardial changes in the tricuspid valve papillary muscles, the right ventricular free wall and the interventricular septum. Similar changes were not seen in control fetuses. Indomethacin administration during pregnancy causes constriction of the fetal ductus arteriosus, fetal pulmonary arterial hypertension, and right ventricular damage. If severe, this may cause rapid fetal death. If less severe, in the newborn infant, this mechanism may be one cause of persistent pulmonary hypertension due to vasoconstriction and increased pulmonary arterial smooth muscle and/or tricuspid insufficiency due to papillary muscle infarction. |
| Databáze: | OpenAIRE |
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