The essential role of arterial pulse in venous return

Abstract

The close proximity of arteries and veins is a well-known anatomical finding documented in the extremities of all vertebrates. However, the physiological consequences of this arrangement are rarely given proper consideration nor are they covered in the textbook list of mechanisms that aid blood flow. We hypothesized that arterial pressure pulsations can significantly increase blood flow in the adjacent valve-containing vein segments. To demonstrate the existence of this mechanism, 10- to 15-cm sections of the bovine forelimb neurovascular bundle were isolated. The proximal and distal ends of the median artery and adjacent veins were cannulated, their tributaries were tied off, and the dissected bundle was then inserted into an airtight enclosure to mimic in vivo encasement by surrounding muscle. Pulsatile pressure was subsequently applied to the arterial segment while recording venous flow. At pressure settings mimicking physiological scenarios, arterial pulsations caused a highly significant increase in venous return. The amplitude of this effect was dependent on the arterial pulsation rate, stroke volume, and pressure gradient across the vein segment.

Keywords: neurovascular bundle; pulse pressure; venous return.

Figure 1.

Bovine forelimb neurovascular bundle (NVB). A: bovine forelimb. Flexor carpi radialis and superficial digital flexor muscles distally to proximally dissected, along with the deep digital flexor muscle. Neuromuscular bundle (NVB) visualized and isolated from surrounding tissue. Six bovine NVBs were used to derive the quantitative and qualitative conclusions discussed in this report. B: blood vessel openings as seen after dissection. Center, artery; sides, veins. C: dissected NVB with marked cannulas (scale bar: 1 cm). D: longitudinal view of crosscut NVB demonstrating multiple valves inside the veins (scale bar: 1 cm).

Figure 2.

Schematics of the experimental setup. A: distal end of the cannulated vein within a tightly wrapped neuromuscular bundle (NVB) was connected to a saline reservoir positioned at different heights. Flow rate was measured by timing the saline weight exiting the proximal end of the vein. A piston pump was used to create rhythmic pulsations inside the artery. B: pressure recordings from an in-line transducer connected to an ADInstruments bridge amplifier were displayed using ADI LabChart software. Impacts of various variables, including pump rate, pump stroke volume, and height of the saline reservoir, were tested using three sequential on/off pump sequences, each lasting 1 min.

Figure 3.

Impact of arterial pulsations on flowrate through the adjacent vein segment. A: open bars correspond to the flowrate in the absence of pulsations. Gray bars indicate flowrate when the arterial pulse was present. The x-axis shows the pressure gradient values across a vertically positioned NVB. The gradient corresponds to the height difference between the saline reservoir and the point where saline exited the vein. The individual experimental values are shown using black dots. B: whisk plot illustrating the impact of pulsation rate on the saline outflow through the vein. The experiment was conducted three times at a 28-mmHg pressure gradient across a vertically positioned NVB. *P < 0.5; **P < 0.01; ***P < 0.001.

Figure 4.

Physiological implications of the observed effect. The graph shows the difference in flowrates through the vein in the absence and presence of the arterial pulse. Individual value points represent the difference between the flowrate in the presence of 70 beats/min pulsations and the average flowrate in absence of pulsations. Top: physiological meaning of the presented quantitative data (see explanation in DISCUSSION).