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. Author manuscript; available in PMC: 2010 Jun 15.
Published in final edited form as: Dev Biol. 2009 Apr 8;330(2):305–317. doi: 10.1016/j.ydbio.2009.03.028

Figure 5.

Figure 5

Histological analysis of HH 35 hearts. (A–A″) PBS-treated control; (B–B″; C–C″) heart treated with 0.6 μg/μl CPA at HH 14; (D–D″) heart treated with 1.0 μg/μl at HH 18. In the control heart (A), the aortic vestibule (AoV) and pulmonary infundibulum (PI) are separated (A) and about the same size. At the valve level, two robust arterial trunks can be seen in the correct orientation. The aorta (Ao) is identified based on its origin from the AoV (A), its posterior position relative to the pulmonary artery (P) at the valve level (A″), and the presence and position of two coronary artery stems from the coronary sinuses (arrows in A″). After CPA treatment at HH 14 (B), a ventricular septal defect allows a connection between the small PI and the AoV (B). The PI disappears before reaching the single outflow vessel (B″). The presence of two coronary arteries penetrating the single outflow vessel further confirms the identity of the Ao (arrows in B″), indicating that this embryo had pulmonary atresia. Another embryo treated at HH 14 (C) exhibits pulmonary atresia. While a ventricular septal defect is present, this defect is very high. The single outflow vessel has five valve leaflets (C″); in addition, two coronary arteries penetrate the aortic side of the single outflow vessel, one of which is seen in C″ (arrow). Treatment at HH 18 (D) results in a well-formed ventricular septum (D), divided arterial valves, (D″) and normal coronary arteries (arrows in D″). Scale bar is 250 μm in A–A″ and 100 μmin A″; the same scales apply to rows B–D.