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

Arterial pulse pressure (PP) increases with exertional stress and ageing, a nd can modify vessel diameter in smaller vessels. To test if PP must exceed a certain range to influence vessel diameter. and determine if such effect s 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 arter ial pressure waveforms. In a separate group of vessels (n = 10), the endoth elium was mechanically removed. Vessel external diameter was measured by vi deo edge-detection. Vessels partially preconstricted with noradrenaline wer e perfused at 9 mL min(-1) mean flow, at mean pressure of 90 or 120 mmHg, a nd zero PP. PP alone was then increased to 40, 70. or 120 mmHg at 1 Hz cycl ing rate for 5 min, then returned to zero and vessel diameter measured imme diately thereafter. The protocol was repeated after 10-20 min stabilization . Mean vessel diameter rose proportionally with PP only once PP exceeded 40 mmHg. with maximal increases of 6-9% at a PP of 120 mmHg. Similar response s were obtained in vessels with and without a functional endothelium, at bo th mean pressures. Thus, when exposed to higher than normal resting PP, con duit arteries dilate owing to the stress-relaxation response of their visco elastic wall. This mechanism of PP-mediated vascular dilatation may contrib ute to enhanced organ perfusion when small resistance arteries are already dilated.