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J. C. B. Jacobsen and C. Aalkjær
i.e. the myogenic mechanism, is important in many tissues to ensure a uniform flow
(flow autoregulation) over a broad range of perfusion pressures. In addition, under
low-pressure conditions accumulation of a diversity of factors in the tissue caused
by inadequate oxygenation and inadequate removal of waste products will enhance
vasodilatation. The latter situation however, unveils the underlying differences in
hydraulic resistance of different flow routes through the network. Consequently, as
pressure is reduced, regions with high resistance may increasingly lose blood-flow
to regions with low resistance.
16.5 Vasomotion Depends on the Hemodynamic Status
and May Have Consequences for Tissue Oxygenation
An interesting observation concerns the relation between perfusion pressure and
the prevalence of flowmotion (cyclic change in blood perfusion, which is a consequence of upstream vasomotion). Smith et al. [50, 51] characterized flowmotion
initiated by pressure reduction in the rabbit gastrocnemius and tenuissimus muscles.
Skeletal muscle tissue displays a well-developed autoregulatory response. Below a
certain pressure limit however, tissue perfusion declines almost linearly with pressure, indicating that perfusion can no longer be sustained by further reduction in
myogenic tone. This lower limit coincides with onset of flowmotion. Reducing the
pressure further enhances flowmotion. However, increased occurrence of flowmotion
is predominantly seen within a certain range of pressures around the lower end of the
autoregulatory curve. Below this range, flowmotion declines and eventually vanishes.
Likely, flowmotion that originate locally in the vascular bed represents oscillations
in vascular tone superimposed on the basal tone ubiquitously present under resting
conditions. Complete loss of basal tone due to very low pressure therefore abolishes
vasomotion altogether. In fact, one would expect flowmotion being absent no matter
the cause of complete vasodilation in a tissue, be it excessively low perfusion pressure, accumulation of metabolites and/or hypoxia. Observations very similar to those
of Smith et al. was made in the rat diaphragm microcirculation, in which vasomotion first become more prevalent during progressive hemorrhagic hypotension, then
decline in prevalence as pressure falls below 60% of normal pressure [6].
Along the same line, a lower perfusion pressure in patients with occlusive peripheral arterial disease (PAD) appears to coincide with a higher prevalence of flowmotion as measured with laser Doppler-flowmetry [24, 46, 52]. Schmidt et al. [52] made
observations in 50 healthy controls and in a total of 75 patients with PAD ranging
in severity from Fontaine class I to class IV (with class IV being the most severe).
Skin flowmotion was relatively rare in healthy subjects (around 10%, mean arterial
pressure in the foot 132 mmHg). Its incidence (plantar side of first toe) increased to
around 50% in class I and II PAD (mean arterial pressure in the foot 100 mmHg)
and on to around 80% in class III and IV PAD (mean arterial pressure in the foot
J. C. B. Jacobsen and C. Aalkjær
i.e. the myogenic mechanism, is important in many tissues to ensure a uniform flow
(flow autoregulation) over a broad range of perfusion pressures. In addition, under
low-pressure conditions accumulation of a diversity of factors in the tissue caused
by inadequate oxygenation and inadequate removal of waste products will enhance
vasodilatation. The latter situation however, unveils the underlying differences in
hydraulic resistance of different flow routes through the network. Consequently, as
pressure is reduced, regions with high resistance may increasingly lose blood-flow
to regions with low resistance.
16.5 Vasomotion Depends on the Hemodynamic Status
and May Have Consequences for Tissue Oxygenation
An interesting observation concerns the relation between perfusion pressure and
the prevalence of flowmotion (cyclic change in blood perfusion, which is a consequence of upstream vasomotion). Smith et al. [50, 51] characterized flowmotion
initiated by pressure reduction in the rabbit gastrocnemius and tenuissimus muscles.
Skeletal muscle tissue displays a well-developed autoregulatory response. Below a
certain pressure limit however, tissue perfusion declines almost linearly with pressure, indicating that perfusion can no longer be sustained by further reduction in
myogenic tone. This lower limit coincides with onset of flowmotion. Reducing the
pressure further enhances flowmotion. However, increased occurrence of flowmotion
is predominantly seen within a certain range of pressures around the lower end of the
autoregulatory curve. Below this range, flowmotion declines and eventually vanishes.
Likely, flowmotion that originate locally in the vascular bed represents oscillations
in vascular tone superimposed on the basal tone ubiquitously present under resting
conditions. Complete loss of basal tone due to very low pressure therefore abolishes
vasomotion altogether. In fact, one would expect flowmotion being absent no matter
the cause of complete vasodilation in a tissue, be it excessively low perfusion pressure, accumulation of metabolites and/or hypoxia. Observations very similar to those
of Smith et al. was made in the rat diaphragm microcirculation, in which vasomotion first become more prevalent during progressive hemorrhagic hypotension, then
decline in prevalence as pressure falls below 60% of normal pressure [6].
Along the same line, a lower perfusion pressure in patients with occlusive peripheral arterial disease (PAD) appears to coincide with a higher prevalence of flowmotion as measured with laser Doppler-flowmetry [24, 46, 52]. Schmidt et al. [52] made
observations in 50 healthy controls and in a total of 75 patients with PAD ranging
in severity from Fontaine class I to class IV (with class IV being the most severe).
Skin flowmotion was relatively rare in healthy subjects (around 10%, mean arterial
pressure in the foot 132 mmHg). Its incidence (plantar side of first toe) increased to
around 50% in class I and II PAD (mean arterial pressure in the foot 100 mmHg)
and on to around 80% in class III and IV PAD (mean arterial pressure in the foot