25 Medical Products Inspired by Biological Oscillators …
391
minute). Although blood is indeed displaced proximally it is the oscillatory nature
of IPC inducing intermittent fluctuations in shear stress to the endothelium that is
now thought to induce further clinical benefits [48].
Human studies on the physiological effects of IPC on circulation have predominantly focused on large vessels such as the popliteal artery [22, 39–40] and vein [23]
in the leg and brachial artery in the arm [56]. Scanning and Doppler ultrasound are
non-invasive techniques that are frequently used to provide measures of large vessel
diameter, blood flow, velocity and also to provide an indirect measure of shear rate on
the vascular endothelium [64, 5], a useful approximation of shear stress that does not
account for blood viscosity. In these large vessels it has been shown that IPC induces
periods of increased arterial inflow [64, 40] and enhanced venous outflow [23] that
have been attributed to both mechanical effects and enhanced shear stress [64, 10].
In summary, IPC intermittently compresses deep compliant veins facilitating venous
emptying by accelerating blood forward, distending that section of the vessel. As
the vessel wall stretches strain occurs in the vascular endothelium with the change
in diameter [10]. Using haemodynamic modelling of flow in a flexible tube, Dai
concluded that an external pressure of 50 mmHg would induce strains at the vessel
lumen border of approximately 20% [19]. In turn, the increase in arterial-venous
pressure gradient significantly increases arterial inflow and hence shear stress to the
vascular endothelium [8]. It is the consequences of these changes in strain and shear
stress to the vascular endothelium induced by IPC that are thought to provide many
of the observed clinical benefits. It is now recognised that the cyclical compression
of IPC increases the shear and compressive strain on the vascular endothelial cells
resulting in the release of biochemical vasoactive mediators [10]. For many decades
compression strain to vessels in the limbs has been associated with a reduction in the
incidence of deep vein thrombosis (DVT) and pulmonary embolism indicative of the
release of anti-thrombotic, pro-fibrinolytic agents [45–17]. The induction of vasodilation by shear stress on vascular endothelial cells has been well documented. In vitro
cell culture systems have demonstrated a rapid release of nitric oxide in response to
shear stress induced by both compression and pulsatile flow [20]. In animal studies
IPC increased the expression of endothelial nitric oxide synthase (eNOS), inhibiting
smooth muscle cells contraction and inducing vasodilation [50–11]. In a rat model
IPC has also been shown to upregulate VEGF mRNA in skeletal muscle but only at
a higher frequency of compressions (2 s on/2 s off) and seemingly independent of
compression pressure [55]. It can therefore be seen that to optimise the clinical benefits of IPC it is important to consider the parameters that influence venous emptying,
arterial inflow and the shear and strain induced in the vascular endothelium. Although
the mechanistic effects of IPC have been studied and clinical benefits reported widely,
single sessions of IPC have not be shown to impact vascular function [64].
Commercial IPC devices have been developed using a wide range of not only
compression pressures but also varying compression cycles (Table 25.1). Readers
are directed to literature reviews on the comparative effectiveness of these devices
[53, 79].
The number of pneumatic compressions per minute has predominantly been determined by the need for adequate venous refilling time following compression [29]
391
minute). Although blood is indeed displaced proximally it is the oscillatory nature
of IPC inducing intermittent fluctuations in shear stress to the endothelium that is
now thought to induce further clinical benefits [48].
Human studies on the physiological effects of IPC on circulation have predominantly focused on large vessels such as the popliteal artery [22, 39–40] and vein [23]
in the leg and brachial artery in the arm [56]. Scanning and Doppler ultrasound are
non-invasive techniques that are frequently used to provide measures of large vessel
diameter, blood flow, velocity and also to provide an indirect measure of shear rate on
the vascular endothelium [64, 5], a useful approximation of shear stress that does not
account for blood viscosity. In these large vessels it has been shown that IPC induces
periods of increased arterial inflow [64, 40] and enhanced venous outflow [23] that
have been attributed to both mechanical effects and enhanced shear stress [64, 10].
In summary, IPC intermittently compresses deep compliant veins facilitating venous
emptying by accelerating blood forward, distending that section of the vessel. As
the vessel wall stretches strain occurs in the vascular endothelium with the change
in diameter [10]. Using haemodynamic modelling of flow in a flexible tube, Dai
concluded that an external pressure of 50 mmHg would induce strains at the vessel
lumen border of approximately 20% [19]. In turn, the increase in arterial-venous
pressure gradient significantly increases arterial inflow and hence shear stress to the
vascular endothelium [8]. It is the consequences of these changes in strain and shear
stress to the vascular endothelium induced by IPC that are thought to provide many
of the observed clinical benefits. It is now recognised that the cyclical compression
of IPC increases the shear and compressive strain on the vascular endothelial cells
resulting in the release of biochemical vasoactive mediators [10]. For many decades
compression strain to vessels in the limbs has been associated with a reduction in the
incidence of deep vein thrombosis (DVT) and pulmonary embolism indicative of the
release of anti-thrombotic, pro-fibrinolytic agents [45–17]. The induction of vasodilation by shear stress on vascular endothelial cells has been well documented. In vitro
cell culture systems have demonstrated a rapid release of nitric oxide in response to
shear stress induced by both compression and pulsatile flow [20]. In animal studies
IPC increased the expression of endothelial nitric oxide synthase (eNOS), inhibiting
smooth muscle cells contraction and inducing vasodilation [50–11]. In a rat model
IPC has also been shown to upregulate VEGF mRNA in skeletal muscle but only at
a higher frequency of compressions (2 s on/2 s off) and seemingly independent of
compression pressure [55]. It can therefore be seen that to optimise the clinical benefits of IPC it is important to consider the parameters that influence venous emptying,
arterial inflow and the shear and strain induced in the vascular endothelium. Although
the mechanistic effects of IPC have been studied and clinical benefits reported widely,
single sessions of IPC have not be shown to impact vascular function [64].
Commercial IPC devices have been developed using a wide range of not only
compression pressures but also varying compression cycles (Table 25.1). Readers
are directed to literature reviews on the comparative effectiveness of these devices
[53, 79].
The number of pneumatic compressions per minute has predominantly been determined by the need for adequate venous refilling time following compression [29]