Cyclooxygenase isoenzymes and patency of ductus arteriosus

Coceani, Flavio; Barogi, Silvia; Brizzi, Francesca; Ackerley, Cameron; Seidlitz, Eric; Kelsey, Lois; Ballou, Leslie R.; Baragatti, Barbara

doi:10.1016/j.plefa.2004.10.004

Cited by 21 publications

(5 citation statements)

References 25 publications

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“…Trivedi et al found increased COX-2 expression with advancing gestation and after birth, and suggested that reduced COX-2 expression in the DA of premature offspring prevented its postnatal constriction [125]. COX-2 may be coupled with downstream microsomal PGE synthases that reinforce its preferential role in prostaglandin production in the DA [62,126]. Chronic pharmacological inhibition of COX-2 mimics COX-2 deletion and also results in PDA [127,128].…”

Section: Molecular Considerations In Pda Pathobiologymentioning

confidence: 99%

“…There are several competing theories that address this apparent contradiction. Some evidence suggests that NO or other vasodilatory mediators are upregulated in the absence of prostaglandins [126]. However, inhibition of NO synthesis did not rescue the PDA phenotype of knockout or chronically COX inhibited mice [128].…”

Section: Molecular Considerations In Pda Pathobiologymentioning

confidence: 99%

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Current Perspectives on Pathobiology of the Ductus Arteriosus

Stoller

DeMauro²,

Dagle³

et al. 2012

J Clin Exp Cardiolog

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The ductus arteriosus (DA) shunts blood away from the lungs during fetal life, but at birth this shunt is no longer needed and the vessel rapidly constricts. Postnatal persistence of the DA, patent ductus arteriosus (PDA), is predominantly a detrimental condition for preterm infants but is simultaneously a condition required to maintain systemic blood flow for infants born with certain severe congenital heart defects. Although PDA in preterm infants is associated with significant morbidities, there is controversy regarding whether PDA is truly causative. Despite advances in our understanding of the pathobiology of PDA, the optimal treatment strategy for PDA in preterm infants is unclear. Here we review recent studies that have continued to elucidate the fundamental mechanisms of DA development and pathogenesis.

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Section: Molecular Considerations In Pda Pathobiologymentioning

confidence: 99%

Section: Molecular Considerations In Pda Pathobiologymentioning

confidence: 99%

Current Perspectives on Pathobiology of the Ductus Arteriosus

Stoller

DeMauro²,

Dagle³

et al. 2012

J Clin Exp Cardiolog

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“…NO acts as an alternative for, and synergizes with, PGE 2 [35] . The NO mechanism is relatively more important in the preterm than in the full-term ductus [36] and can compensate for PG-induced relaxation when PG biosynthesis is eliminated or inhibited by drugs [37,38] . In their in vitro and in vivo studies using wild-type and gene-deleted mice, Baragatti et al [35] described NO and CO as being cooperative mediators of bradykinin-induced relaxation in the absence of PGE 2. In the absence of all three agents Fig.…”

Section: Physiology and Pharmacology Of Constriction And Relaxationmentioning

confidence: 99%

Insights into the Pathogenesis and Genetic Background of Patency of the Ductus Arteriosus

Bökenkamp¹,

DeRuiter²,

Munsteren³

et al. 2009

Neonatology

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The unique differentiation program of the ductus arteriosus (DA) is essential for its specific task during fetal life and for the adapting circulation after birth. Phenotypic changes occur in the DA during the normal maturation and definitive closure. Morphological abnormalities of the vessel wall characterize the persistent DA (PDA) in older children. Here, we give an overview of the animal models of DA regulation and remodeling. Genetic research has identified the cause of syndromic forms of PDA, such as the TFAP2B mutations in Char syndrome. Genes that interfere with the remodeling of vascular smooth muscle cells (VSMCs) of the ductal media are affected in virtually all of these anomalies. Therefore, the pivotal regulatory role of VSMCs is emphasized. A better understanding of the genetic background of this developmental process may help develop new strategies to manipulate the DA in premature infants, neonates with duct-dependent anomalies, and patients with syndromic and non-syndromic PDA.

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“…If it remains open after birth, a condition known as patent DA (PDA) would happen [2,3]. PDA develops at a notable frequency of more than 40% in preterm infants with birth weight of 1500 g or less [4,5].…”

Section: Introductionmentioning

confidence: 99%