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C. Thorn and A. Shore
is in agreement with the findings of a study where transcutaneous oxygen tension
was monitored at the skin surface during IPC and the partial pressure of oxygen in the
skin was shown to significantly increase [4]. Furthermore the enhanced blood flow
induced by IPC has also been observed by capillaroscopy to increase the capillary
density in the skin [74]. Research on the effects of IPC on skeletal muscle perfusion
shows some similarities with the well-known exercise induced hyperaemia observed
following a single muscle contraction [42, 14]. Contract-induced rapid onset vasodilation results from a rapid increase in blood flow within the first second attributed
to an acute mechanical effect of muscle contraction (muscle pump) followed by
an additional active dilatation of resistance vessels [65, 76] induced by vasoactive
metabolites released from contracting fibres [67–18] and the vascular endothelium
[18]. Endothelial signalling pathways induce upstream vasodilation in feed arteries
known as conducted vasodilation [67]. The relative contribution of the muscle pump
versus interstitial or endothelial vasodilators to this contract-induced vasodilation is
still a matter of debate. In studies in rat muscle IPC has been shown to increase the
production of endothelial vasodilator nitric oxide [72, 11]. The upregulation of eNOS
mRNA not only occurred in compressed muscle but also in adjacent uncompressed
muscle and it is suggested that this is induced by IPC-mediated shear stress. The
upregulation of VEGF mRNA in rat skeletal muscle by IPC suggests it may also
encourage new vessel growth and improved perfusion. Single impulse cuff inflation
to 200 mmHg to the forearm muscle has also been shown to evoke vasodilation in
the muscle bed increasing the forearm vascular compliance [36].
Intermittent pneumatic compression has therefore found a range of clinical applications both from the improved venous return and the effects of changing shear stress
and strain on the vascular endothelium. These mechanisms not only induce vasodilation but also induce a cascade of biochemical responses which downregulate the
expression of adhesion molecules, inflammatory and chemokine genes; and promote
the inhibition of white blood cell adhesion and platelet aggregation [7, 13, 16]. It
can therefore be seen that IPC devices can activate physiological mechanisms that
have a wide range of clinical applications. Intermittent pneumatic compression is a
well-established technique in the management of advanced chronic venous disease,
specifically venous ulceration [46, 16, 6]. The IPC devices can enhance venous return
and prevent stasis, especially where valves are not compromised. Exploiting the many
biochemical response induced by IPC has led to it also being widely used for the
prevention of deep venous thrombosis (DVT) and pulmonary embolism [47, 34, 12]
both during surgery [47, 79, 34, 26] and whilst on bed rest. In 11 non-orthopaedic
surgical randomised controlled trials, IPC reduced the incidence of asymptomatic
DVT from 25% in the control group to 7.9% in the IPC group [47]. In 11 multimodality studies, combining IPC with anticoagulant medication further decreased the
incidence of DVT from 4.1% with IPC alone to 2.19% with IPC and pharmacological
prophylaxis [34].
IPC systems have also been shown to reduce oedema [10] and are therefore used
in the treatment of lymphedema [78, 61]. This reduction in oedema through IPC
has further been shown to increase dermal oxygen tension [38], possibly through
C. Thorn and A. Shore
is in agreement with the findings of a study where transcutaneous oxygen tension
was monitored at the skin surface during IPC and the partial pressure of oxygen in the
skin was shown to significantly increase [4]. Furthermore the enhanced blood flow
induced by IPC has also been observed by capillaroscopy to increase the capillary
density in the skin [74]. Research on the effects of IPC on skeletal muscle perfusion
shows some similarities with the well-known exercise induced hyperaemia observed
following a single muscle contraction [42, 14]. Contract-induced rapid onset vasodilation results from a rapid increase in blood flow within the first second attributed
to an acute mechanical effect of muscle contraction (muscle pump) followed by
an additional active dilatation of resistance vessels [65, 76] induced by vasoactive
metabolites released from contracting fibres [67–18] and the vascular endothelium
[18]. Endothelial signalling pathways induce upstream vasodilation in feed arteries
known as conducted vasodilation [67]. The relative contribution of the muscle pump
versus interstitial or endothelial vasodilators to this contract-induced vasodilation is
still a matter of debate. In studies in rat muscle IPC has been shown to increase the
production of endothelial vasodilator nitric oxide [72, 11]. The upregulation of eNOS
mRNA not only occurred in compressed muscle but also in adjacent uncompressed
muscle and it is suggested that this is induced by IPC-mediated shear stress. The
upregulation of VEGF mRNA in rat skeletal muscle by IPC suggests it may also
encourage new vessel growth and improved perfusion. Single impulse cuff inflation
to 200 mmHg to the forearm muscle has also been shown to evoke vasodilation in
the muscle bed increasing the forearm vascular compliance [36].
Intermittent pneumatic compression has therefore found a range of clinical applications both from the improved venous return and the effects of changing shear stress
and strain on the vascular endothelium. These mechanisms not only induce vasodilation but also induce a cascade of biochemical responses which downregulate the
expression of adhesion molecules, inflammatory and chemokine genes; and promote
the inhibition of white blood cell adhesion and platelet aggregation [7, 13, 16]. It
can therefore be seen that IPC devices can activate physiological mechanisms that
have a wide range of clinical applications. Intermittent pneumatic compression is a
well-established technique in the management of advanced chronic venous disease,
specifically venous ulceration [46, 16, 6]. The IPC devices can enhance venous return
and prevent stasis, especially where valves are not compromised. Exploiting the many
biochemical response induced by IPC has led to it also being widely used for the
prevention of deep venous thrombosis (DVT) and pulmonary embolism [47, 34, 12]
both during surgery [47, 79, 34, 26] and whilst on bed rest. In 11 non-orthopaedic
surgical randomised controlled trials, IPC reduced the incidence of asymptomatic
DVT from 25% in the control group to 7.9% in the IPC group [47]. In 11 multimodality studies, combining IPC with anticoagulant medication further decreased the
incidence of DVT from 4.1% with IPC alone to 2.19% with IPC and pharmacological
prophylaxis [34].
IPC systems have also been shown to reduce oedema [10] and are therefore used
in the treatment of lymphedema [78, 61]. This reduction in oedema through IPC
has further been shown to increase dermal oxygen tension [38], possibly through