Several arteries course through the posterior abdominal wall. The aorta passes the aortic hiatus at T12 level through the diaphragm and descends anterior to the vertebral column. The aorta branches into the right and left common iliac arteries at L4. The aorta gives rise to the inferior phrenic arteries just below the aortic hiatus. These vessels supply the diaphragm and also give rise to the suprarenal vessels. The renal arteries arise from the aorta just inferior to the origin of the superior mesenteric artery. The right renal artery is longer and a little inferior to the left renal artery and traverses behind the inferior vena cava (IVC). The left renal artery passes posterior to the left renal vein. Testicular or ovarian arteries descend into the retroperitoneum and run laterally on the psoas major muscle and across the ureter. The testicular artery accompanies the ductus deferens into the scrotum. Here it provides blood to the epididymis, testis, and spermatic cord. The ovarian artery traverses through the suspensory ligament of the ovary, supplies the ovary, and anastomosis with the ovarian branch of the uterine artery. Lumbar arteries consist of 4 or 5 pairs that originate from the back of the aorta. These vessels need to be ligated when performing aortic aneurysm surgery. They run posterior to the sympathetic trunk, the IVC (on the right side), the quadratus lumborum, and psoas major muscles. The lumbar vessels give off numerous small anterior branches and accompany the dorsal primary rami of the corresponding spinal nerves and divide into spinal and muscular branches. The middle sacral artery comes off the posterior of the aorta, just above the bifurcation; the vessel then runs down the anterior of the sacrum and ends at the coccygeal body. It supplies the anal canal and rectum and joins the superior and inferior rectal arteries. In the posterior abdominal wall, other important vessels that are not arteries include: IVC is formed by the union of the 2 common iliac veins just to the right of L5. The bifurcation of the IVC is almost always lower than the bifurcation of the aorta in the pelvis. As it ascends, the IVC remains to the right of the aorta. At the diaphragm, it ascends through the IVC hiatus at T8 and enters the right atrium. Through its course, it receives venous blood from the adrenals, renal veins, right gonads, hepatic veins, and inferior phrenic veins. The cisterna chyli, formed by the lumbar and intestinal lymphatics, lies just posterior and to the right of the aorta. It is usually located between the two crura of the diaphragm and ascends through the aortic hiatus in the diaphragm.  The cisterna chyli is the inferior collecting sac of the thoracic duct which returns chyle to the venous system at the left brachiocephalic vein, where the left subclavian and left internal jugular veins converge. The para-aortic lymph nodes can be divided into subgroups which include the preaortic, retroaortic and lateral aortic groups. The preaortic nodes are located next to the origin of the celiac trunk, superior and inferior mesenteric arteries. Surgeons, radiologists, and other health professionals need to be familiar with these vessels as multiple pathologic conditions may develop resulting in untoward consequences from vessel injury.

Numerous studies have begun to unravel the genetic basis of not only aortic disease but also other forms of commonly encountered vascular diseases. The goal of this review is to provide clinicians a reference to help identify and diagnose different types of vascular disease with a genetic underpinning.

Licochalcone A (LA), a chalcone derived from liquorice, exhibits multiple biological activities, including anti-oxidation and anti-inflammation. This study aimed to investigate the role and underlying mechanism of LA in the abdominal aortic aneurysm (AAA). AAA model was established by continuous infusion of 1000 ng/kg/min of angiotensin II (AngII) in ApoE -/- mice for 4 weeks. At 7 days before AngII administration, 5 mg/kg/day or 10 mg/kg/day of LA was intraperitoneally administered to mice and continued for 4 weeks. The characteristics and quantification of AAAs were determined in situ. Real-time PCR or western blot was used to measure mRNA or protein levels of matrix metalloproteinase 2 and matrix metalloproteinase 9; pro-inflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6; apoptosis-related proteins Bax, Bcl-2, and active caspase-3; miR-181b; Sirtuin 1 (SIRT1); and heme oxygenase-1 (HO-1). Mouse-aorta-origin vascular smooth muscle (MOVAS) cells were used to confirm the involved pathways in vitro. We found LA administration dose-dependently reduced the incidence of AngII-induced AAA, aneurysm diameter enlargement, elastin degradation, matrix metalloproteinase production, pro-inflammatory cytokines and miR-181b expression, and vascular smooth muscle cell apoptosis. It elevated SIRT1 and HO-1 expression that was suppressed by AngII. AngII enhanced miR-181b but reduced SIRT1 and HO-1 expression in MOVAS cells. In AngII-stimulated MOVAS cells, downregulation of miR-181b significantly upregulated the expression of SIRT1 and HO-1, the effect of which was abrogated by SIRT1 siRNA. Collectively, LA could attenuate AngII-induced AAA by modulating the miR-181b/SIRT1/HO-1 signaling. LA might be a potential medical therapy for small AAA.

Aneurysm is a multifactorial degenerative disease characterized by focal dilatation of blood vessels. Although abdominal aortic (AAA) and popliteal aneurysms (PAA) are the most common dilatative vascular diseases and share some features, a comparison between the different anatomical sites and the relative pathophysiological differences has not been established. In order to gain deeper insights to AAA and PAA, we have characterized the role of matrix remodelling, vascular cells phenotype depletion and the inflammatory process in both diseases. Results show a more extensive presence of T-cell, B-cell and monocyte-macrophage infiltration in AAA with respect to PAA. Concurring with this aspect, IL-6, IL-8 and MCP-1 are 10-fold increased in AAA. Moreover, MMP-9, and metalloproteinase inhibitor 3 (TIMP3) resulted up-regulated in AAA tissues. Regarding the catalytic activity, which is tightly related to the oxidative stress, we found an up-regulation of superoxide dismutase [Mn] mitochondrial (SODM), glutathione peroxidase 3 (GPX3) and peroxiredoxin-1 (PRDX1). Histological analyses clearly showed a massive elastin fragmentation in AAA. This may enhance the inflammatory response, which has a prevalent role in AAA, while PAA is mainly guided by a loss of the contractile phenotype. These findings suggest insight in these potentially devastating diseases in term of their progression, aiming to identify potential specific markers respectively for AAA and PAA treatment.