title: Linked opening angle and histological and mechanical aspects of the proximal pulmonary arteries of healthy and pulmonary hypertensive rats and calves.
abstract: Understanding how arterial remodeling changes the mechanical behavior of pulmonary arteries (PAs) is important to the evaluation of pulmonary vascular function. Early and current efforts have focused on the arteries' histological changes, their mechanical properties under in vitro mechanical testing, and their zero-stress and no-load states. However, the linkage between the histology and mechanical behavior is still not well understood. To explore this linkage, we investigated the geometry, residual stretch, and histology of proximal PAs in both adult rat and neonatal calf hypoxic models of pulmonary hypertension (PH), compared their changes due to chronic hypoxia across species, and proposed a two-layer mechanical model of artery to relate the opening angle to the stiffness ratio of the PA outer to inner layer. We found that the proximal PA remodeling in calves was quite different from that in rats. In rats, the arterial wall thickness, inner diameter, and outer layer thickness fraction all increased dramatically in PH and the opening angle decreased significantly, whereas in calves, only the arterial wall thickness increased in PH. The proposed model predicted that the stiffness ratio of the calf proximal PAs changed very little from control to hypertensive group, while the decrease of opening angle in rat proximal PAs in response to chronic hypoxia was approximately linear to the increase of the stiffness ratio. We conclude that the arterial remodeling in rat and calf proximal PAs is different and the change of opening angle can be linked to the change of the arterial histological structure and mechanics.
authors.affiliation: Department of Mechanical Engineering, University of Colorado, Boulder, Colorado, USA.
authors.forename: Lian
authors.initials: L
authors.lastname: Tian
authors.forename: Steven R
authors.initials: SR
authors.lastname: Lammers
authors.forename: Philip H
authors.initials: PH
authors.lastname: Kao
authors.forename: Mark
authors.initials: M
authors.lastname: Reusser
authors.forename: Kurt R
authors.initials: KR
authors.lastname: Stenmark
authors.forename: Kendall S
authors.initials: KS
authors.lastname: Hunter
authors.forename: H Jerry
authors.initials: HJ
authors.lastname: Qi
authors.forename: Robin
authors.initials: R
authors.lastname: Shandas
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001696:Biomechanical Phenomena; D001794:Blood Pressure; D002417:Cattle; D004195:Disease Models, Animal; D055119:Elastic Modulus; D065627:Familial Primary Pulmonary Hypertension; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D000860:Hypoxia / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D008955:Models, Cardiovascular; D011651:Pulmonary Artery / Q000473:pathology* / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013045:Species Specificity; D013314:Stress, Mechanical