The role of elastin in pulmonary hypertensive conduit artery stiffening.

摘要

Proximal pulmonary arterial stiffness directly affects the efficiency and load imposed on the heart muscle during the cardiac cycle and is an important predictor of cardiovascular mortality in hypertensive patients. The pulsatile nature of the heart pump cycle necessitates distensible conduit arteries for maintaining coronary perfusion and steady blood flow throughout the capillary bed. Pulmonary hypertension causes material property changes, which affect conduit pulmonary artery compliance through vascular remodeling of the conduit pulmonary arteries.The biological and structural changes which occur in arterial tissue in response to hypertension are not completely understood. We determined that there was a need to ascertain the impact of pulmonary hypertension on the continuum and bulk mechanical properties of the structural protein elastin. Our studies use a large mammalian calf model, which closely approximates human physiology. We used mechanical testing of both fresh tissue and purified elastin from normotensive and hypertensive groups to facilitate comparisons based on pathology as well as physiology. These results were then used to experimentally verify the mechanics and load bearing role of elastin in passive conduit pulmonary arterial tissues in an effort to answer our hypothesis: that changes in the structure and material properties of elastin, resulting from pulmonary hypertension, cause a significant increase in the stiffness of the proximal pulmonary arteries.