Arterial Stenosis Causes Remodeling and Reactivity Changes in Pre and Post Segments

Vascular stenosis or narrowing may occur in disease, injury or mismatch in vascular graft diameter. The left carotid artery was stenosed 30% of original diameter in sheep (n=3) under anesthesia. Flow and diameter measurements were obtained before and 15 weeks after stenosis. Pre‐ and post‐stenotic segments of carotid artery were dissected and compared to right carotid artery (control). Using standard tissue baths, arterial rings were constricted with potassium chloride (118 mM) and Norepinephrine (0.3 μM) and tension was measured in g/g. Following norepinephrine constriction, arterial rings were relaxed with acetylcholine or S‐nitrosyl aminopenicillamine (SNAP, nitric oxide donor). Arterial rings were stretched incrementally and recorded as length‐tension slope. The maximal tension (break tension) was recorded as kg tension per g arterial ring weight. Histological studies using H & E, Masson's trichrome (for collagen) and van Giessen (for elastin) stains were done. Data are shown as mean ± SD. Post‐stenotic segments constrict poorly to norepinephrine and relax better to acetyl choline (endothelium dependent relaxing agent) compared to pre‐stenotic segments. Relaxation responses to SNAP (endothelium independent relaxing agent) are similar. This suggests an upregulation of endothelial nitric oxide release in the post‐stenotic segment. Both pre‐ and post‐stenotic segments stretch poorly (low slope on length‐tension curves) and break more easily compared to control artery. Supported by Department of Pediatrics, Women and Children's Hospital of Buffalo