Angioarchitecture of the venous and capillary system in heart defects induced by retinoic acid in mice.
BACKGROUND
Corrosion casting and immunohistochemical staining with anti-alpha smooth muscle actin and anti-CD34 was utilized to demonstrate the capillary plexus and venous system in control and malformed mouse hearts.


METHODS
Outflow tract malformations (e.g., double outlet right ventricle, transposition of the great arteries, and common truncus arteriosus) were induced in progeny of pregnant mice by retinoic acid administration at day 8.5 of pregnancy.


RESULTS
Although control hearts exhibited areas in which capillaries tended to be oriented in parallel arrays, the orientation of capillaries in the respective areas of malformed hearts was chaotic and disorganized. The major branch of a conal vein in control hearts runs usually from the left side of the conus to its right side at the root of the pulmonary trunk and opens to the right atrium below the right auricle; thus, it has a curved course. On the other hand, a conal vein in malformed hearts courses from the left side or from the anterior side of the conus and tends to traverse straight upwards along the dextroposed aorta or along the aortopulmonary groove with its proximal part located outside of the heart. Other cardiac veins in outflow tract malformations are positioned in the same locations as in control hearts.


CONCLUSIONS
We postulate that the changed location of the conal vein and disorganized capillary plexus result from malformed morphogenesis of the outflow tract and/or a disturbed regulation of angiogenic growth factor release from the adjacent environment.
Ratajska
Anna
A
Department of Pathological Anatomy, Medical University of Warsaw, Chałubińskiego 5, Warsaw 02-004,Poland. arataj@ib.amwaw.edu.pl
Ciszek
Bogdan
B
Zajaczkowska
Agnieszka
A
Jabłońska
Anna
A
Juszyński
Michał
M
D000818:Animals; D002196:Capillaries / Q000002:abnormalities; D003330:Coronary Vessel Anomalies / Q000139:chemically induced / Q000473:pathology* / Q000648:ultrastructure; D004195:Disease Models, Animal; D005260:Female; D006330:Heart Defects, Congenital / Q000139:chemically induced; D051379:Mice; D008807:Mice, Inbred BALB C; D008962:Models, Theoretical; D011247:Pregnancy; D014212:Tretinoin; D014680:Veins / Q000002:abnormalities / Q000187:drug effects
D014212:Tretinoin