title: Stenotic amplification of vasoconstriction responses.
abstract: Based on simple hemodynamic principles, arterial stenoses could accentuate the effects of arterial vasoconstriction by reducing intraluminal pressure. To examine this mechanism we employed an in vitro stenotic carotid artery preparation. Eight carotid arteries, obtained from anesthetized heartworm-positive dogs, were isolated and perfused with a physiological salt solution under constant pressure (100 mmHg) and with a fixed distal resistance. After creating an intraluminal stenosis, proximal pressure, distal pressure, and flow were continuously recorded as norepinephrine was incrementally added to the perfusion reservoir. At each norepinephrine concentration, arterial dimensions were recorded on 35-mm film and measured by quantitative dimensional analysis. These data were approximated by a four-parameter logistic equation. The proximal diameter data were considered to represent solely the effects of arterial vasoconstriction, while the stenotic diameter data were considered to be affected both by arterial vasoconstriction and by stenotic pressures. The stenotic diameters shortened significantly more than the proximal diameter (1.2 +/- 2 vs. 0.5 +/- 0.1 mm, P less than 0.01). The shape of the stenotic diameter dose-response curve was similar to the distal pressure curve and was significantly (P less than 0.05; - 3.4 +/- 0.7) steeper than the proximal diameter curve (-0.7 +/- 0.1). Furthermore, the half maximum effective doses (ED50) were significantly interrelated for distal pressure and stenotic diameter data and unrelated for proximal diameter data. In five additional experiments, to eliminate the stenotic pressure changes, the flow was maintained constant. Maintaining stenotic vasoconstriction response (0.6 +/- 2 mm). The results of the present study show exaggerated stenotic vasoconstriction caused by a stenotic pressure decrease.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Section of Cardiology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103.
authors.forename: K
authors.initials: K
authors.lastname: Li
authors.forename: W P
authors.initials: WP
authors.lastname: Santamore
authors.forename: D L
authors.initials: DL
authors.lastname: Morley
authors.forename: T N
authors.initials: TN
authors.lastname: Tulenko
mesh_terms: D000818:Animals; D002339:Carotid Arteries / Q000503:physiopathology; D002340:Carotid Artery Diseases / Q000503:physiopathology*; D003251:Constriction, Pathologic / Q000503:physiopathology; D004285:Dogs; D006439:Hemodynamics; D066298:In Vitro Techniques; D009638:Norepinephrine / Q000097:blood; D014655:Vascular Resistance; D014661:Vasoconstriction
chemical_list: D009638:Norepinephrine