Effects of mean and pulsatile wall shear stress on the diameter of the iliac artery in the anaesthetized pig

R Kelly and HM Snow. (Introduced by E.Johns) Biological Services Unit and Department of Physiology, University College Cork, Cork, Ireland.

Two forces affect the endothelium of conduit arteries, namely shear stress and circumferential stress resulting from blood flow and pressure respectively. These two forces have a mean and a pulsatile component. Results from previous experiments in the dog (Snow et al 2001) have shown that increases in mean wall shear stress (MSS) causes endothelium dependent dilatation of large conduit arteries mediated by nitric oxide (NO). In contrast, it was suggested that the pulsatile component of shear stress (PSS) caused constriction. However, this effect of PSS was based upon a statistical interpretation of pooled results and in no single experiment was a clear cut constrictor effect of PSS observed. Furthermore the design of the above experiments in the dog meant that increases in PSS could not be separated from concomitant increases in arterial pulsatile pressure. We have re-examined the effects of PSS in the iliac artery of the pig using a preparation which allows independent control of MSS and PSS without causing significant changes in arterial pressure.

Experiments were carried out in 6 anaesthetized female landrace pigs (wt mean±sd 26.5±2.2 kg: induction, pentobarbitone 30mg/kg i.v., maintenance 6mg/kg/h i.v.) ventilated (40% oxygen in air) via a tracheostomy. Arterial blood pressure (strain gauge transducer), blood flow (ultrasonic transit time flowmeter) and diameter (sonomicrometry) of the left iliac artery were measured and digitally recorded (PowerLab Chart 5). The distal ends of the left iliac artery and vein were connected by a shunt which incorporated a variable resistance and a capacitor (‘windkessel’) enabling precise regulation of the mean and amplitude of pulsatile blood flow. MSS and PSS were calculated from measurements of arterial diameter, blood flow and blood viscosity. The effects of stepwise increases in blood flow and hence MSS on arterial diameter were recorded in the presence and absence of the capacitor i.e. with maximum and minimum PSS. In 6 pigs the mean control blood flow was 77 ±8.4 ml.min-1 and was increased to 727±140ml.min-1(means±S.E.M) and the corresponding changes in diameter were 3.7±0.33mm to 4.32±0.33mm (means±S.E.M). In the presence of minimum PSS (7.68 ±3.08N.m2 (mean±S.E.M)) the sensitivity of the effect of an increase in MSS on the increase in diameter (measured as the change in diameter per unit change in MSS) was 0.176±0.05mm/N.m2 and in the presence of maximum PSS (23.68±5.24N.m2) was significantly (p<0.05 paired t) reduced to 0.136±0.05mm/N.m2 (means±S.E.M). Changing PSS had no significant effects on mean and pulsatile blood pressure.

In conclusion these results in the pig confirm that increases in mean wall shear stress (MSS) are an important stimulus for the release of NO by the endothelium as indicated by changes in arterial diameter and that increases in the amplitude of the pulsatile component of shear stress (PSS) have a small but significant inhibitory effect on this response. They also corroborate the hypothesis that the uneven distribution of atheroma throughout the arterial system is related to the ratio of pulsatile to mean shear stress and consequent variability in the production of NO.

Snow,H.M. et al (2001), Journal of Physiology, 531.3, pp 843-848.