16 Mechanism and Consequence of Vasomotion
267
75 mmHg). Furthermore, with other factors matched, skin oxygenation appeared to
be better in the presences of flowmotion as compared to a situation without [49].
Similar observations were made by Hudetz et al. [25] in the rat cerebral circulation
which also has a pronounced autoregulatory response. Reduction in mean arterial
pressure by various methods below 90 mmHg all resulted in appearance of flow oscillations at 4–11 cpm, the amplitude of which grew with further pressure reduction.
Time-averaged flow was preserved though, corresponding in this case to an intact
autoregulation. Oscillations were completely abolished during cerebral vasodilatation by 5% carbon dioxide in the inspired air. Abolition of all tone by lowering
pressure to very low levels was not investigated in that study, however Fujii et al.
[11] found that pronounced hypotension abolishes vasomotion in another cerebral
vessel, the basilar artery (for a review see [26]).
The abovementioned studies identified an association between pressure reduction
and the prevalence of flowmotion, but this does not guarantee a direct causal relation
between the two. Rather, some evidence point to the state within the tissue itself
as a main determinant of the prevalence and characteristics of flowmotion. In the
observations above from both rabbit and man, flowmotion became more prevalent
as perfusion pressure was reduced. While this could be a consequence of the pressure reduction itself and its effect on the arterial wall it could also be a consequence
of reduced perfusion, in turn changing the state of the tissue. That factors such as
reduction in oxygen transport to the tissue may be as important a stimulus as the
pressure reduction itself, was shown by Lee et al. [36]. They observed that the prevalence of flowmotion (around 3 cpm) increased from 65% under baseline conditions
to 100% during hemodilution to 43% of normal hematocrit, which is equivalent to a
large reduction in the oxygen transport capacity of the blood. Thorn et al. [56] noted
when simultaneously recoding flow and oxygenation in the skin microcirculation
of healthy individuals, that there appears to be distinct modes of flowmotion. One
of these oscillations involves a fall in oxygenated hemoglobin and a simultaneous
rise in deoxygenated hemoglobin. Further investigation [55], revealed what could
potentially be a causal relation inducing flowmotion. A slow decline in blood mean
oxygen saturation (reflected in a simultaneous rise in deoxygenated hemoglobin and
fall in oxygenated hemoglobin) to a threshold value induced a consistent and rapid
rise in flow, which was again followed by a slow decline. A possible interpretation
of this pattern is that the tissue under resting conditions cyclically upregulates its
own flow when a certain critical lower limit is approached. This must somehow
involve upstream signaling, likely in the form of an electrical vascular conducted
response running in the endothelium, from the capillary bed to the upstream resistance network in order to allow for a rapid and consistent increase in flow. To that end,
laser-Doppler-flowmetry of flowmotion in the rabbit tenuissimus muscle has indeed
been found to correlate tightly with vasomotion in upstream transverse arterioles
[50].
In a different tissue, the rat testis, Lysiak et al. [37] measured flow and oxygen
tension (with laser Doppler-flowmetry and an oxygen electrode) simultaneously in
the interstitium and found the two signals to be completely phase-locked at 12 cpm
267
75 mmHg). Furthermore, with other factors matched, skin oxygenation appeared to
be better in the presences of flowmotion as compared to a situation without [49].
Similar observations were made by Hudetz et al. [25] in the rat cerebral circulation
which also has a pronounced autoregulatory response. Reduction in mean arterial
pressure by various methods below 90 mmHg all resulted in appearance of flow oscillations at 4–11 cpm, the amplitude of which grew with further pressure reduction.
Time-averaged flow was preserved though, corresponding in this case to an intact
autoregulation. Oscillations were completely abolished during cerebral vasodilatation by 5% carbon dioxide in the inspired air. Abolition of all tone by lowering
pressure to very low levels was not investigated in that study, however Fujii et al.
[11] found that pronounced hypotension abolishes vasomotion in another cerebral
vessel, the basilar artery (for a review see [26]).
The abovementioned studies identified an association between pressure reduction
and the prevalence of flowmotion, but this does not guarantee a direct causal relation
between the two. Rather, some evidence point to the state within the tissue itself
as a main determinant of the prevalence and characteristics of flowmotion. In the
observations above from both rabbit and man, flowmotion became more prevalent
as perfusion pressure was reduced. While this could be a consequence of the pressure reduction itself and its effect on the arterial wall it could also be a consequence
of reduced perfusion, in turn changing the state of the tissue. That factors such as
reduction in oxygen transport to the tissue may be as important a stimulus as the
pressure reduction itself, was shown by Lee et al. [36]. They observed that the prevalence of flowmotion (around 3 cpm) increased from 65% under baseline conditions
to 100% during hemodilution to 43% of normal hematocrit, which is equivalent to a
large reduction in the oxygen transport capacity of the blood. Thorn et al. [56] noted
when simultaneously recoding flow and oxygenation in the skin microcirculation
of healthy individuals, that there appears to be distinct modes of flowmotion. One
of these oscillations involves a fall in oxygenated hemoglobin and a simultaneous
rise in deoxygenated hemoglobin. Further investigation [55], revealed what could
potentially be a causal relation inducing flowmotion. A slow decline in blood mean
oxygen saturation (reflected in a simultaneous rise in deoxygenated hemoglobin and
fall in oxygenated hemoglobin) to a threshold value induced a consistent and rapid
rise in flow, which was again followed by a slow decline. A possible interpretation
of this pattern is that the tissue under resting conditions cyclically upregulates its
own flow when a certain critical lower limit is approached. This must somehow
involve upstream signaling, likely in the form of an electrical vascular conducted
response running in the endothelium, from the capillary bed to the upstream resistance network in order to allow for a rapid and consistent increase in flow. To that end,
laser-Doppler-flowmetry of flowmotion in the rabbit tenuissimus muscle has indeed
been found to correlate tightly with vasomotion in upstream transverse arterioles
[50].
In a different tissue, the rat testis, Lysiak et al. [37] measured flow and oxygen
tension (with laser Doppler-flowmetry and an oxygen electrode) simultaneously in
the interstitium and found the two signals to be completely phase-locked at 12 cpm