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Understanding the pathobiology in patent ductus arteriosus in prematurity-beyond prostaglandins and oxygen.

08:00 EDT 9th April 2019 | BioPortfolio

Summary of "Understanding the pathobiology in patent ductus arteriosus in prematurity-beyond prostaglandins and oxygen."

The ductus arteriosus (DA) is probably the most intriguing vessel in postnatal hemodynamic transition. DA patency in utero is an active state, in which prostaglandin E (PGE) and nitric monoxide (NO), play an important role. Since the DA gets programmed for postnatal closure as gestation advances, in preterm infants the DA frequently remains patent (PDA). PGE exposure programs functional postnatal closure by inducing gene expression of ion channels and phosphodiesterases and anatomical closure by inducing intimal thickening. Postnatally, oxygen inhibits potassium and activates calcium channels, which ultimately leads to a rise in intracellular calcium concentration consequently inducing phosphorylation of the myosin light chain and thereby vasoconstriction of the ductus arteriosus. Since ion channel expression is lower in preterm infants, oxygen induced functional vasoconstriction is attenuated in comparison with full term newborns. Furthermore, the preterm DA is more sensitive to both PGE and NO compared to the term DA pushing the balance toward less constriction. In this review we explain the physiology of DA patency in utero and subsequent postnatal functional closure. We will focus on the pathobiology of PDA in preterm infants and the (un)intended effect of antenatal exposure to medication on both fetal and neonatal DA vascular tone.

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This article was published in the following journal.

Name: Pediatric research
ISSN: 1530-0447
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Medical and Biotech [MESH] Definitions

A congenital heart defect characterized by the persistent opening of fetal DUCTUS ARTERIOSUS that connects the PULMONARY ARTERY to the descending aorta (AORTA, DESCENDING) allowing unoxygenated blood to bypass the lung and flow to the PLACENTA. Normally, the ductus is closed shortly after birth.

A syndrome of persistent PULMONARY HYPERTENSION in the newborn infant (INFANT, NEWBORN) without demonstrable HEART DISEASES. This neonatal condition can be caused by severe pulmonary vasoconstriction (reactive type), hypertrophy of pulmonary arterial muscle (hypertrophic type), or abnormally developed pulmonary arterioles (hypoplastic type). The newborn patient exhibits CYANOSIS and ACIDOSIS due to the persistence of fetal circulatory pattern of right-to-left shunting of blood through a patent ductus arteriosus (DUCTUS ARTERIOSUS, PATENT) and at times a patent foramen ovale (FORAMEN OVALE, PATENT).

A chromosome disorder associated with TRISOMY of all or part of CHROMOSOME 13. Clinical manifestations include CONGENITAL HEART DEFECTS (e.g., PATENT DUCTUS ARTERIOSUS), facial malformations (e.g., CLEFT LIP; CLEFT PALATE; COLOBOMA; MICROPHTHALMIA); HYPOTONIA, digit malformations (e.g., POLYDACTYLY or SYNDACTYLY), and SEIZURES and severe INTELLECTUAL DISABILITY associated with NERVOUS SYSTEM MALFORMATIONS.

A fetal blood vessel connecting the pulmonary artery with the descending aorta.

A condition caused by underdevelopment of the whole left half of the heart. It is characterized by hypoplasia of the left cardiac chambers (HEART ATRIUM; HEART VENTRICLE), the AORTA, the AORTIC VALVE, and the MITRAL VALVE. Severe symptoms appear in early infancy when DUCTUS ARTERIOSUS closes.

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