Validation of a pressure diameter method for determining modulus and strain of collagen engagement for long branches of bovine pulmonary arteries.

Recent studies have shown that capacitance measurements of large arteries provide better prognosis and diagnosis than tests of resistance alone in pulmonary hypertension (Mahapatra et al., 2006, "Relationship of Pulmonary Arterial Capacitance and Mortality in Idiopathic Pulmonary Arterial Hypertension," J. Am. Coll. Cardiol., 47(4), pp. 799-803; Reuben, 1971, "Compliance of the Human Pulmonary Arterial System in Disease," Circ. Res., 29, pp. 40-50]. Decreased arterial capacitance causes increased load to the heart and is the direct result of increased stiffness and elastic modulus of the arterial wall. Here, we validate a pressure-diameter (PD) method for comparing the elastic modulus and collagen engagement for post-hilar pulmonary arteries with a large range of arterial diameter. The tissue mechanics of the post-hilar arteries are not well-characterized in pulmonary hypertension. It is believed that future studies with this method will provide useful insight into the role of passive tissue mechanics of these arteries in the pathophysiology of pulmonary hypertension, eventually improving clinical diagnosis, prognosis, and treatment. Post-hilar pulmonary arteries, excised from healthy and hypertensive calves and healthy cows, were inflated over a range of 0 [mm Hg] to 110 [mm Hg] in an isolated tissue bath. Internal pressure was recorded with an electric pressure catheter. Artery diameter and longitudinal stretch were recorded photographically. Stress-strain data curves were extracted using Lame's law of thick-walled tubes. Radial strips were removed from each section and tested in a uniaxial (MTS) tester for validation. Both the elastic modulus and collagen engagement strain were similar to results obtained by more traditional means. The average difference between measured values of the two methods for collagen engagement strain was 3.3% of the average value of the engagement strain. The average difference between the measured values of the two methods for modulus of elasticity was 7.4% of the average value of the modulus. The maximum, theoretical, relative error for the stress determined with the PD method was calculated at 20.3%. The PD method proved to be a suitable replacement for uniaxial strain tests in comparing collagen engagement strains. The method allowed faster testing of tissues of multiple diameters, while removing the effect of end conditions. The PD method will be of further utility in continued study of tissue mechanics in pulmonary hypertension studies.

Linked opening angle and histological and mechanical aspects of the proximal pulmonary arteries of healthy and pulmonary hypertensive rats and calves.

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.