In a new extension of the Cardiovascular model we have explored the possible collaboration of arterial acceleration on the one hand and the release and spread of endothelium derived relaxing factor (EDRF) on blood circulation within a confined tree of branching arteries. These arteries have been modeled by capacitances connected with resistances. The first simulation demonstrates how the pulsatile signal of heart contraction in the more proximal branches is transformed to a continuous flow in the most distal branches.
The explanation for this is that any volume of blood driven into the capacitance on the left has three options: 1. remain in this capacitance, 2. flow over a resistance into the next capacitance up right or 3. flow over a resistance into the next capacitance down right. During systole blood is temporarily stored in the capacitance and is released during diastole. Since in a steady state total blood flow at the left (systole plus diastole) equals the summed capillary outflow at the far left, the temporary storage of volume during systole followed by its gradual release during diastole causes dampening of the outflow at every additional node of the arterial tree.
The second simulation shows that an increase in tissue pressure is an important obstacle for the non-pulsatile flow at the level of the capillaries. Blood flow will chose the path of least resistance and can easily bypass segments of the arterial tree under less favourable conditions.
The third simulation shows how arterial acceleration enhances pulsatility of capillary outflow. In the model arterial acceleration is simulated by a temporary and shortlasting decrease in capacitance at stroke onset, causing the capacitance to resist expansion for a brief moment in time. In the model the triggering of arterial acceleration is synchronous for all capacitances from left to right, forcing blood out of the arterial tree during the first 100-150 ms of each heart beat.
Thereby, arterial acceleration augments the increase in intraluminal pressure at stroke onset (upstroke) which is thought to result in the release of EDRF. In the simulation more EDRF is indicated by a more intense yellow colour. After turning the arterial acceleration on, its effect on blood flow and on the production of EDRF is shown by a systolic peak during early systole and a pulsatile colouring of the arterial branches. EDRF is a free radical (with chemical formula NO or nitric oxide) that is deactivated ultrafast. In the model the tau of exponential decay is set to 3 s, meaning that the concentration is reduced to a factor 1/e within 3 s. So, EDRF has little chance to build up in the capacitances and its concentration will modulated synchronously to the beating heart.
Arterial acceleration has more penetration power, meaning that it is more likely to persist when tissue pressure increases. This too is modeled by selecting nodes in the arterial tree (turning to orange), selecting tissue pressure on and gradually moving the slider mid below to the right. As explained elsewhere on these pages, the increase in tissue pressure makes the flow velocity signal more Sys1 (= arterial acceleration) dominant.
With arterial acceleration active, the flow velocity waveform changes from Sys2 exclusive at the far left, via Sys2 dominant, Sys12 balanced, Sys1 dominant to Sys1 exclusive in the nodes with increased tissue pressure at the far right.
In the case of increased tissue pressure, arterial acceleration may overcome the resistance to blood flow. However, when nothing further happens, tissue perfusion remains fully dependent on arterial acceleration. This is where EDRF comes in: tissues at elevated tissue pressures will still receive the Sys1 pulse of arterial acceleration. With the heart pulse meeting a higher resistance to flow, more EDRF will be released and transported into the distal branches by a wave of arterial acceleration. Now EDRF instigates dilatation of these more distant arterial branches allowing blood to flow in during also late systole and diastole. This is demonstrated in the next simulation.
In this simulation the release of EDRF is correlated with the strength of arterial acceleration. This is demonstrated by the simulation below. When arterial acceleration increases it also increases EDRF causing vessels to open up and allow the arterial acceleration to reach into the vessels further downstream. This makes the combination of arterial acceleration and EDRF even more potent in allowing blood to flow into distal capillary systems than arterial acceleration alone.
On a larger scale this explains how the combination of arterial acceleration and EDRF work together to make blood flow within the arterial branches more homogenous: when a large resistance to blood flow is met, more EDRF is produced and transported into the more distal branches by a wave of arterial acceleration, whereas a low vascular resistance causes less production of EDRF, allowing more distal branches to increase their resistance. This is simulated below. Different nodes have been selected with an increase in tissue pressure. It shows how the release of EDRF opens up some and closes down other distal branches of the tree.
