Angiogenic proteins in the lungs of children after cavopulmonary anastomosis

Starnes, Sandra L.; Duncan, Brian W.; Kneebone, James M.; Rosenthal, Geoffrey L.; Patterson, Kathleen; Fraga, Charles H.; Kilian, Karen; Mathur, Sanjeev Kumar; Lupinetti, Flavian M.

doi:10.1067/mtc.2001.115423

Cited by 38 publications

(32 citation statements)

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“…After cavopulmonary anastomosis, pulmonary microvessel density is increased even in the absence of clinically apparent pulmonary arteriovenous malformations, supporting the presence of constant angiogenic stimuli (40). Lung biopsy specimens from children after cavopulmonary anastomosis had increased expression of VEGF and its receptor (41).The mechanism whereby the pulmonary circulation processes IL-8 and the potential role of IL-8 in the pathogenesis of angiogenesis warrant further study.…”

Section: Accepted Manuscriptmentioning

confidence: 92%

Aspirin resistance in adult patients after Fontan surgery

Tomkiewicz‐Pająk¹,

Wójcik²,

Chłopicki³

et al. 2015

International Journal of Cardiology

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Section: Accepted Manuscriptmentioning

confidence: 92%

Aspirin resistance in adult patients after Fontan surgery

Tomkiewicz‐Pająk¹,

Wójcik²,

Chłopicki³

et al. 2015

International Journal of Cardiology

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“…Clinically heparin has been used in the patients associated with congenital heart disorders because development of pulmonary vascular bed is mandatory prior to open-heart surgery in order to achieve successful clinical outcome (Geggal et al 1990;Starnes et al 2000Starnes et al , 2001. Heparin administration to these patients above induce vascular proliferation, which could contribute to cordial operation.…”

Section: Discussionmentioning

confidence: 99%

“…Heparin administration to these patients above induce vascular proliferation, which could contribute to cordial operation. Heparin is also considered to be involved in the regulation of neonatal pulmonary artery development chiefly through its ability to promote angiogenesis in conjunction with various growth factors (Leopald et al 1998;Starnes et al 2001). However it is also true that its angiogenesis-promoting effects were not necessarily well characterized.…”

Section: Discussionmentioning

confidence: 99%

Heparin Accelerates Pulmonary Artery Development in Neonate Rabbits

Watanabe

Suzuki

Shizawa

et al. 2005

Tohoku J. Exp. Med.

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Pulmonary vascular resistance drops sharply within a few minutes after birth for the survival of neonates. A majority of this resistance is caused by "pulmonary vascular bed" or vessel lacking smooth muscle cells. Heparin is known to promote proliferation and development of endothelial cells and to subsequently decrease their overall vascular resistance, but its detailed features remained unknown. Therefore, in this study we treated neonatal rabbits with heparin, protamine (antagonist of heparin), or saline, and evaluated histopathological features of vascular endothelial cells using two different types of computer assisted image analysis, i.e., CAS200 and NIH image. These two systems detected the percentage of vascular endothelial area per fields (VA) and CD31-positive area per total area of tissue following subtraction of background stain. CD31 was used as an endothelial cell marker. Heparin treated rabbits were associated with significant decrement of pulmonary/systemic artery pressure (Pp/Ps) (21.0 ± 6.0%) compared to protamine (29.9 ± 6.1%) or saline (29.4 ± 3.0%) treated animals. The values of VA obtained by the two image analyses (CAS200 and NIH image) were significantly increased in heparin treated animals (38.4 ± 3.2% determined by CAS200 and 24.0 ± 1.3% by NIH image) compared to protamine (30.2 ± 3.9% and 19.2 ± 1.8%) or saline (33.2 ± 1.5% and 20.8 ± 3.8%) treated animals on 14th day of treatment. The present study indicates that heparin accelerates pulmonary vascular bed development probably by increasing the number and volume of endothelial cells, which subsequently contributes to the decrease in pulmonary vascular resistance. pulmonary artery vascular resistance; pulmonary vascular density; heparin; CD31; image analysis

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“…[20] For example, in a clinical study, Jabbour and colleagues reported that a higher proliferation rate in endothelial cells isolated from cerebral arteriovenous malformations was associated with increased levels of vascular endothelial growth factor (VEGF)-A and VEGF receptors [21]. Recent findings from clinical and experimental studies have implicated similar pro-angiogenic processes to be operative in PAVM development in the post-SCPC setting [22].…”

Section: Introductionmentioning

confidence: 99%

“…[37] While angiogenic pathways have been recognized in many normal and pathologic physiologic processes including arterio-venous malformations,[20,21,31] there are currently no established molecular mechanisms that have been linked to PAVM formation. The lack of understanding of molecular mechanisms may explain the absence of non-surgical, non-invasive, treatment(s) for PAVMs.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary arteriovenous malformations after the superior cavopulmonary shunt: mechanisms and clinical implications

Kavarana

Jones

Stroud

et al. 2014

Expert Review of Cardiovascular Therapy

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Children with functional single ventricle heart disease are commonly palliated down a staged clinical pathway toward a Fontan completion procedure (total cavopulmonary connection). The Fontan physiology is fraught with long term complications associated with lower body systemic venous hypertension, eventually resulting in significant morbidity and mortality. The bidirectional Glenn shunt or superior cavopulmonary connection (SCPC) is commonly the transitional stage in single ventricle surgical management and provides excellent palliation. Some studies have demonstrated lower morbidity and mortality with the SCPC when compared with the Fontan. Unfortunately the durability of the SCPC is significantly limited by the development of pulmonary arteriovenous malformations (PAVMs) which have been commonly attributed to the absence of hepatic venous blood flow and the lack of pulsatile flow to the affected lungs. Abnormal angiogenesis has been suggested as a final common pathway to PAVM development. Understanding these fundamental mechanisms through the investigation of angiogenic pathways associated with the pathogenesis of PAVMs would help to develop medical therapies that could prevent or reverse this complication following SCPC. Such therapies could improve the longevity of the SCPC, potentially eliminate or significantly postpone the Fontan completion with its associated complications, and improve long-term survival in children with single ventricle disease.

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Angiogenic proteins in the lungs of children after cavopulmonary anastomosis

Cited by 38 publications

References 0 publications

Aspirin resistance in adult patients after Fontan surgery

Aspirin resistance in adult patients after Fontan surgery

Heparin Accelerates Pulmonary Artery Development in Neonate Rabbits

Pulmonary arteriovenous malformations after the superior cavopulmonary shunt: mechanisms and clinical implications

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