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Articles in PresS, published online ahead of print July 11, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00368.2002
Submitted on April 25, 2002
Accepted on July 9, 2002
1 Surgery, University of Washington, Seattle, Washington, USA
2 Pediatric & Congenital Heart Surgery, Cleveland Clinic Foundation, Cleveland, Ohio, USA
3 Pediatrics, University of Washington, Seattle, Washington, USA
* To whom correspondence should be addressed. E-mail: duncanb{at}ccf.org.
Objective: We developed a rat model of pulmonary arteriovenous malformations after cavopulmonary anastomosis. We sought to determine whether this model reproduces the angiographic and histologic features seen in the human condition. Methods: Eight Sprague Dawley rats underwent a right superior cavopulmonary anastomosis using microsurgical techniques. Between 2 and 13 months postoperatively, pulmonary angiography was performed, the animals were sacrificed and the lungs were removed. Microscopic sections of the lung were stained with an endothelial-specific antibody(von Willibrand Factor). Microvessel density was determined by counting vessels positively staining for von Willibrand Factor and the shunted and non-shunted(control)lungs were compared for each animal. Results: Pulmonary angiography revealed time-dependent development of arteriovenous malformations. Microvessel density demonstrated a time-dependent increase in the shunted lung compared to the control lung(simple linear regression of the ratio of the microvessel density of the shunted lung divided by the microvessel density of the control lung on time; R square= 0.79, p= 0.003. Conclusion: This animal model reproduces the same angiographic and microscopic features of pulmonary arteriovenous malformations that develop in humans after cavopulmonary anastomosis. This appears to be a valid model that may be used to further study etiologic mechanisms for this phenomenon.
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