Lung antioxidant enzymes are regulated by development and increased pulmonary blood flow.

Increasing data suggest that oxidative stress, due to an increased production of reactive oxygen species and/or a decrease in antioxidants, is involved in the pathophysiology of pulmonary hypertension. Several antioxidant systems regulate the presence of oxidant species in vivo, and of primary interest are the superoxide dismutases (SOD) and catalase. However, little is known about the expression of antioxidant enzymes during the development of pulmonary hypertension.

Increased oxidative stress in lambs with increased pulmonary blood flow and pulmonary hypertension: role of NADPH oxidase and endothelial NO synthase.

Although oxidative stress is known to contribute to endothelial dysfunction-associated systemic vascular disorders, its role in pulmonary vascular disorders is less clear. Our previous studies, using isolated pulmonary arteries taken from lambs with surgically created heart defect and increased pulmonary blood flow (Shunt), have suggested a role for reactive oxygen species (ROS) in the endothelial dysfunction of pulmonary hypertension, but in vivo data are lacking. Thus the initial objective of this study was to determine whether Shunt lambs had elevated levels of ROS generation and whether this was associated with alterations in antioxidant capacity.

Improving the results of small-bore vascular graft testing in rabbits: a technical primer.

Appropriate models to evaluate the in vivo behavior of small-diameter grafts are varied. To evaluate the behavior of small-diameter, bovine-derived grafts in the arterial circulation, we chose the rabbit abdominal aorta model. In the development of our procedure, we evaluated several models published in the literature, with unsatisfactory results.

Cellular expression of PCNA and procollagen in vital and ethanol-treated autologous pericardial implants in sheep.

Background And Aims Of The Study: Cardiovascular surgeries involving repair or reconstruction of heart valve leaflets with vital autologous pericardium have shown detrimental healing outcomes, mainly fibrosis with retraction. It is proposed that cells intrinsic to the pericardial implants may contribute to this fibrosis by becoming activated to proliferate and synthesize type I collagen.

Methods: Vital and ethanol-treated autologous pericardium were implanted as rectangular flaps bisecting the lumen in the descending aorta of sheep to simulate a heart valve leaflet.

An in vitro model of pericardial tissue healing.

Introduction: A previous study in our laboratory showed that a flap of fresh autologous pericardium bisecting the aorta of sheep retracted and became fibrotic. Histologic analyses suggested that activated cells within the pericardium contributed to the retraction of the implant. Here we report the development of an in vitro model to investigate the effects of serum on cellular proliferation and cell-mediated tissue contraction.

Serum components stimulate pericardial tissue contraction.

Background And Aims Of The Study: Previous experiments have demonstrated the retraction and fibrosis of vital autologous pericardial flap implants in the descending aorta of sheep. An in-vitro model of pericardial tissue contraction was developed that showed healing reactions similar to those observed in the fresh in-vivo flap. Here, the component(s) of serum that stimulate tissue contraction were partially characterized.