>In your presentation you describe that SHR display blunted flow-induced mesenteric collateral artery remodeling. These animals are known to display also an impaired flow-induced dilatation. The question now arises whether impaired remodeling is a direct consequence of endothelial-dysfunction or the result of modified local hemodynamics. The contribution of Debbie Ceiler and myself to this symposium demonstrates that pharmacologically-induced endothelial dysfunction (chronic L-NAME) persistently blocks shunting of blood flow through the collateral channels. These findings favor a hemodynamic hypothesis (remodeling would not occur because the flow does not go up).
>What were the flows in your SHR experiment?
Dear Dr. De Mey,
Collateral blood flow was doubled in both the normal and SHR animals. The primary mechanism for this increase in blood flow within our model has been demonstrated to be an increased pressure gradient from the boundary region to the center of the collateral dependent region (Unthank et al.). If impaired flow-induced dilation was indeed present in our SHR animals then our data further supports this concept of increased collateral blood flow in our model.
In small resistance arteries, an increase in blood flow does not necessarily produce an increase in shear. Therefore, we believe that the shear rates are more important in understanding hemodynamic stimuli than actual flows. Shear rates were significantly increased in our collateral vessels as shown in Figure 2. Thus we believe our data clearly indicate that the SHR collateral vessels have impaired shear-induced remodeling.