Sustained vessel dilation induced by increased pulsatile perfusion of porcine carotid arteries in vitro

F. A. Recchia, B. J. Byrne, David A. Kass

Research output: Contribution to journalArticle

Abstract

Arterial pulse pressure (PP) increases with exertional stress and ageing, and can modify vessel diameter in smaller vessels. To test if PP must exceed a certain range to influence vessel diameter, and determine if such effects are endothelium-dependent or intrinsic to vascular viscoelasticity, eight fresh excised porcine carotid artery segments were perfused with modified Krebs-Henseleit by a servo-controlled system generating physiological arterial pressure waveforms. In a separate group of vessels (n = 10), the endothelium was mechanically removed. Vessel external diameter was measured by video edge-detection. Vessels partially preconstricted with noradrenaline were perfused at 9 mL min-1 mean flow, at mean pressure of 90 or 120 mmHg, and zero PP. PP alone was then increased to 40, 70, or 120 mmHg at 1 Hz cycling rate for 5 min, then returned to zero and vessel diameter measured immediately thereafter. The protocol was repeated after 10-20 min stabilization. Mean vessel diameter rose proportionally with PP only once PP exceeded 40 mm Hg, with maximal increases of 6-9% at a PP of 120 mmHg. Similar responses were obtained in vessels with and without a functional endothelium, at both mean pressures. Thus, when exposed to higher than normal resting PP, conduit arteries dilate owing to the stress-relaxation response of their viscoelastic wall. This mechanism of PP-mediated vascular dilatation may contribute to enhanced organ perfusion when small resistance arteries are already dilated.

Original languageEnglish (US)
Pages (from-to)15-21
Number of pages7
JournalActa Physiologica Scandinavica
Volume166
Issue number1
DOIs
StatePublished - Jun 8 1999

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Keywords

  • Blood pressure
  • Endothelium
  • Pulsatile
  • Vascular biology
  • Viscoelasticity

ASJC Scopus subject areas

  • Physiology

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