Valveless, tubular pumps are widespread in the animal kingdom, but the mechanism by which these pumps generate fluid flow is often in dispute. Where the pumping mechanism of many organs was once described as peristalsis, other mechanisms, such as dynamic suction pumping, have been suggested as possible alternative mechanisms. Peristalsis is often evaluated using criteria established in a technical definition for mechanical pumps, but this definition is based on a small-amplitude, long-wave approximation which biological pumps often violate. In this study, we use a direct numerical simulation of large-amplitude, short-wave peristalsis to investigate the relationships between fluid flow, compression frequency, compression wave speed, and tube occlusion. We also explore how the flows produced differ from the criteria outlined in the technical definition of peristalsis. We find that many of the technical criteria are violated by our model: Fluid flow speeds produced by peristalsis are greater than the speeds of the compression wave; fluid flow is pulsatile; and flow speed have a nonlinear relationship with compression frequency when compression wave speed is held constant. We suggest that the technical definition is inappropriate for evaluating peristalsis as a pumping mechanism for biological pumps because they too frequently violate the assumptions inherent in these criteria. Instead, we recommend that a simpler, more inclusive definition be used for assessing peristalsis as a pumping mechanism based on the presence of non-stationary compression sites that propagate unidirectionally along a tube without the need for a structurally fixed flow direction.
Keywords: Embryonic heart; Fluid dynamics; Peristalsis.