A biophysical and histological analysis of factors that lead to aortic rupture in normal and lathyritic turkeys

Abstract

These experiments were designed to determine if local differences in elastic properties or wall structure contributed to the development of aortic rupture in turkeys. Static elastic properties were measured from pressure-volume curves of cylindrical segments of upper and lower thoracic aorta and innominate artery in two groups of lathyritic birds and two age-matched control groups. The biggest changes were in the young lathyritic group that was on 0.04% beta-aminoproprionitrile at 3 weeks of age and continued for 2, 3, or 4 weeks. Much smaller changes were seen in the older group that started on 0.05% beta-aminoproprionitrile at 6 weeks of age for 10 days and then 0.02% beta-aminoproprionitrile for the next 9-12 weeks. The biggest changes were seen in the abdominal aorta, which ruptured spontaneously in 50% of the young lathyritic group. The birds had a marked decrease in the number of elastin layers per unit wall thickness. Analysis of the elastic diagrams showed that the elastance of both elastin and collagen were altered in the young lathyritic group. Rupture appeared to follow partial dissection of plaques, but true longitudinal dissection did not occur.

Insights on the Pathogenesis of Aneurysm through the Study of Hereditary Aortopathies

“…However, other studies have shown that collagen deposition, especially in the adventitial layer, can be protective and part of beneficial "scar repair" mechanisms preventing transmural ruptures [71,375,393,394]. Consistent with these latter observations, genetic or pharmacological inactivation of lysyl oxidases, enzymes necessary for collagen and elastin cross-linking, cause or exacerbate aneurysm in patients and animal models [197,198,246,255,269,273,[395][396][397]. The detrimental effects of fluoroquinolones on TAA pathogenesis have also been attributed to excess ECM degradation and reduced levels of collagen [398][399][400][401].…”

“…These results raised the possibility that AT 1 R signaling might have protective effects in TAA, both directly and through the enhancement of any protective effects of TGF-β signaling [367,451]. For example, the inhibition of AT 1 R-dependent collagen deposition and maturation, directly or through TGF-β-dependent pathways, could recapitulate, in part the detrimental effect of lysyl oxidase inhibition with β-amino-propionitrile (BAPN), which causes dissection or rupture in a number of animal models [255,[395][396][397]414,415,417,452,453]. Additionally, AT 1 R-dependent signaling could be beneficial through stimulation of VSMC contraction [367,454].…”