A large part of it is due to the complexity of controlled regression in the dorsal aortae, vitelline arteries, and the ventral anastomotic artery.
First, a preface: During development from days 8-23, the aorta are paired dorsal structures in the embryo which communicate through a ventral anastomotic artery.
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| Days 8-23 of the fetus, the dorsal aortae have two ventral branches which are connected via a ventral anastomotic artery that usually disappears during differentiation (not shown). (ref 2) |
Then around day 30, the dorsal aortae fuse... by day 36 the ventral branches fuse...
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| Diagram showing the fused ventral branches / vitelline branches out of which the celiac, superior mesenteric, and inferior mesenteric arteries form (10th, 13th, and 21st/22nd branches) though controlled regression of the remaining branches. (ref 2). |
And then, when all the structures are fused at midline, a controlled regression takes place to form the mesenteric arteries we're all familiar with... but sometimes the regression doesn't always go the way it's expected to...
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| A diagram highlighting some of the various configurations that the celiac artery and the SMA can take through abnormal regression of the segmental branches and ventral anastomotic artery. (A) is the configuration before regression. Configuration (F) is the Arc of Buhler (see the 10/4/12 post). (ref 1) |
In addition to controlled regression of ventral/vitelline arteries, the orientation of mesenteric arteries is also influenced by the positioning of other organs. For instance, the inferior pancreaticoduodenal artery typically arises from the right side of the SMA, but the SMA also rotates 180 degrees during development. If this fails to happen -- in addition to malrotation of the gut -- the inferior pancreaticoduodenal artery can arise from the left side of the artery.
Although the molecular pathways of angiogenesis and embryogenesis are still being worked out, some results point to the Notch/VEGF pathway as perhaps a fundamental signalling cascade in the differentiation of arterial from venous structures, and perhaps it plays a role in the controlled regression of the vitelline arteries as well?
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1. Walker TG. "Mesenteric Vasculature and Collateral Pathways." Semin Intervent Radiol. 2009 September; 26(3): 167–174.
2. Hardman RL, Lopera JE, Cardan RA, et al. "Common and Rare Collateral Pathways in Aortoiliac Occlusive Disease: A Pictorial Essay" AJR:197, September 2011.
3. "Gastrointenstinal Angiography" Reuter, Redman, Cho. 3rd ed (1986)
