16 Mechanism and Consequence of Vasomotion
269
pressure. The intervention could be a situation with abolition of vasomotion versus
control. Clearly, this requires that we fully understand the pathways which leads to
vasomotion (and consequently flowmotion), in order to selectively block vasomotion without affecting tissue metabolism by the intervention itself. Such data would
provide valuable input to the discussion of the consequences of vasomotion.
There are numerous examples of spontaneous or induced vasomotion in isolated
vessels (e.g. Peng et al. [43], Gustafsson et al. [17, 20], Broegger et al. [5], Rahman
et al. [45], reviewed in [2]). Since isolated vessels are devoid of influence from other
vessels, nerves and surrounding tissue, self-sustained oscillations must, as noted
above, be an intrinsic property of the vascular wall. The ubiquitous presence of
vasomotion across species and tissues suggests that, rather than being a question
of ability per se to oscillate it is a question of which set of conditions should be
present for a given type of vessel to oscillate. Thus, the oscillatory ability may or
may not, be evoked under the specific conditions that prevail in a given tissue at a
given time. Simulation studies show that myogenic reactivity in a network of vessels
may in itself be enough to elicit complex and self-sustained oscillatory behavior [57],
and, as discussed above, indeed intraluminal pressure has been shown to modulate
vasomotion characteristics [3]. When it comes to causal relations and consequences
however, it is helpful that some studies report the occurrence of flowmotion (as the
consequence of vasomotion) together with independently measured parameters such
as tissue oxygenation or tracer clearance. For instance, it appears that flowmotion
become more prevalent and pronounced as autoregulation reaches its lower limit,
perfusion heterogeneity increases and the tissue experiences risk of focally insufficient oxygenation. In some tissues, a life on the edge of insufficient flow appear
be the normal state although likely for different reasons in different tissues. In the
skin, minimal perfusion under baseline conditions could be an adaptation to avoid
heat-loss at rest, whereas in the testis it may, as described above, represent a specific
adaptation to avoid high oxygen pressures. Whatever the reason, the tissue faces the
same problem: with a heterogeneous distribution network, approaching the lower
limit of sufficient perfusion increases the risk of some regions experiencing hypoxia
for periods intolerable for the tissue cells. In this situation however, the different
stimuli (e.g. accumulation of metabolites, fall in pH, fall in oxygen tension) seem
to increasingly converge to push the vascular wall from a non-oscillatory and into
an oscillatory domain. While, as outlines above, an oscillating flow may increase
the local delivery of oxygen and drainage of the interstitium, it may also have a
more direct effect. By periodically forcing the hydraulic resistance up in some parts
of the network and simultaneously down in others, flow is forced along constantly
shifting flow routes (briefly reviewed in [28]). In this way the effect of structural
heterogeneity in the network is mitigated and the risk of some tissue areas experiencing long-lasting hypoxia or ischemia is reduced. Below a certain critical perfusion
pressure however, total flow is insufficient to match total tissue demand in all cases.
Eventually, as shown by Schmidt [49] and others, vasomotion/flowmotion tend to
disappear when pressure becomes very low. In this situation, where the microvascular bed relaxes completely due to absence of myogenic activation and buildup of
tissue waste products, flowmotion would probably be of little significance anyway.
269
pressure. The intervention could be a situation with abolition of vasomotion versus
control. Clearly, this requires that we fully understand the pathways which leads to
vasomotion (and consequently flowmotion), in order to selectively block vasomotion without affecting tissue metabolism by the intervention itself. Such data would
provide valuable input to the discussion of the consequences of vasomotion.
There are numerous examples of spontaneous or induced vasomotion in isolated
vessels (e.g. Peng et al. [43], Gustafsson et al. [17, 20], Broegger et al. [5], Rahman
et al. [45], reviewed in [2]). Since isolated vessels are devoid of influence from other
vessels, nerves and surrounding tissue, self-sustained oscillations must, as noted
above, be an intrinsic property of the vascular wall. The ubiquitous presence of
vasomotion across species and tissues suggests that, rather than being a question
of ability per se to oscillate it is a question of which set of conditions should be
present for a given type of vessel to oscillate. Thus, the oscillatory ability may or
may not, be evoked under the specific conditions that prevail in a given tissue at a
given time. Simulation studies show that myogenic reactivity in a network of vessels
may in itself be enough to elicit complex and self-sustained oscillatory behavior [57],
and, as discussed above, indeed intraluminal pressure has been shown to modulate
vasomotion characteristics [3]. When it comes to causal relations and consequences
however, it is helpful that some studies report the occurrence of flowmotion (as the
consequence of vasomotion) together with independently measured parameters such
as tissue oxygenation or tracer clearance. For instance, it appears that flowmotion
become more prevalent and pronounced as autoregulation reaches its lower limit,
perfusion heterogeneity increases and the tissue experiences risk of focally insufficient oxygenation. In some tissues, a life on the edge of insufficient flow appear
be the normal state although likely for different reasons in different tissues. In the
skin, minimal perfusion under baseline conditions could be an adaptation to avoid
heat-loss at rest, whereas in the testis it may, as described above, represent a specific
adaptation to avoid high oxygen pressures. Whatever the reason, the tissue faces the
same problem: with a heterogeneous distribution network, approaching the lower
limit of sufficient perfusion increases the risk of some regions experiencing hypoxia
for periods intolerable for the tissue cells. In this situation however, the different
stimuli (e.g. accumulation of metabolites, fall in pH, fall in oxygen tension) seem
to increasingly converge to push the vascular wall from a non-oscillatory and into
an oscillatory domain. While, as outlines above, an oscillating flow may increase
the local delivery of oxygen and drainage of the interstitium, it may also have a
more direct effect. By periodically forcing the hydraulic resistance up in some parts
of the network and simultaneously down in others, flow is forced along constantly
shifting flow routes (briefly reviewed in [28]). In this way the effect of structural
heterogeneity in the network is mitigated and the risk of some tissue areas experiencing long-lasting hypoxia or ischemia is reduced. Below a certain critical perfusion
pressure however, total flow is insufficient to match total tissue demand in all cases.
Eventually, as shown by Schmidt [49] and others, vasomotion/flowmotion tend to
disappear when pressure becomes very low. In this situation, where the microvascular bed relaxes completely due to absence of myogenic activation and buildup of
tissue waste products, flowmotion would probably be of little significance anyway.