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 language | English (US) |
|---|---|
| Pages (from-to) | 15-21 |
| Number of pages | 7 |
| Journal | Acta Physiologica Scandinavica |
| Volume | 166 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1999 |
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Keywords
- Blood pressure
- Endothelium
- Pulsatile
- Vascular biology
- Viscoelasticity
ASJC Scopus subject areas
- Physiology
Cite this
Sustained vessel dilation induced by increased pulsatile perfusion of porcine carotid arteries in vitro. / Recchia, F. A.; Byrne, B. J.; Kass, David A.
In: Acta Physiologica Scandinavica, Vol. 166, No. 1, 1999, p. 15-21.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Sustained vessel dilation induced by increased pulsatile perfusion of porcine carotid arteries in vitro
AU - Recchia, F. A.
AU - Byrne, B. J.
AU - Kass, David A
PY - 1999
Y1 - 1999
N2 - 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.
AB - 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.
KW - Blood pressure
KW - Endothelium
KW - Pulsatile
KW - Vascular biology
KW - Viscoelasticity
UR - http://www.scopus.com/inward/record.url?scp=0033001032&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033001032&partnerID=8YFLogxK
U2 - 10.1046/j.1365-201x.1999.00532.x
DO - 10.1046/j.1365-201x.1999.00532.x
M3 - Article
VL - 166
SP - 15
EP - 21
JO - Acta Physiologica Scandinavica
JF - Acta Physiologica Scandinavica
SN - 0370-839X
IS - 1
ER -