The effect of shear stress induced nitric oxide production on dynamic compliance in the iliac artery of the anaesthetised pig

Kelly RF & Snow HM*. Hatter Institute for Cardiology Research , Chris Barnard Building, University of Cape Town, Cape Town, South Africa.*Dept of Physiology, University College Cork, Cork, Ireland.

Recent studies ( Wilkinson et al, 2002) measuring pulse wave velocity , have shown that flow mediated dilatation increases the dynamic distensibility of conduit arteries. Pulse wave velocity is now used as a non-invasive index of the ability of the endothelium to respond to increases in wall shear stress, produce nitric oxide and cause arterial dilatation. However, distensibility is related to both the artery diameter and dynamic elastic modulus of the wall. The purpose of the present investigation was to make direct estimates of dynamic elastic modulus by measuring diameter and pressure in the iliac artery, using a shunt preparation which allowed precise control of blood flow ( Kelly & Snow, 2006). The effect of increases in wall shear stress and consequent vasodilatation on dynamic elasticmoduluswere measured in 5 female landrace pigs of weight 24-31kg (Induction, pentobarbitone 30mg/kg i.v., maintenance 6mg/kg/hr). Dynamic elastic modulus was calculated from plots of pressure against diameter throughout 3 cardiac cycles and expressed as Youngs modulus (Nm-2) which is defined as the ratio of the increase in tension to the fractional increase in diameter, where fractional increases in diameter is equal to the change in diameter divided by the lowest diameter during diastole. Tension in the wall (kNm-2) normalized for wall thickness (mm) was calculated from pressure (mmHg) and diameter (mm) ;

Tension=(pressurex 0.133)x((diameter/2)/wall thickness).

Youngs modulus was then obtained as the slope of the plots of tension vs fractional increase in diameter using linear regression analysis. The mean control level of Youngs modulus at low shear stress was 3538 +/- 404 kN.m-2 and at high shear stress was 3069+/- 454 kN.m-2 the difference of -470 +/- 177 kN.m-2 is significant ( p<0.05, paired t, n=10). The corresponding change in diameter was an increase from 3.584+/-0.383 mm to 3.871+/-0.217mm, an increase of 0.713+/-0.257 which was significant (p<0.05, paired t, n=10). There was an overall 19% decrease in Youngs modulus for a 28% increase in diameter. When these experiments were repeated in the presence of 20mg/kg L-NAME i.v. there was no increase in diameter in response to shear stress. These results show that flow mediated release of nitric oxide increases artery diameter and reduces dynamic elastic modulus, both actions contributing to the reduction of pulse wave velocity.

Kelly & Snow (2005). http://www.pa2online.org/abstracts/Vol3Issue4abst015Phtml
Wilkinson et al (2002). Circulation. 105, 213-219.