17 Biological Oscillations of Vascular Origin and Their Meaning …
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related to arteriolar diameter, because the smallest arterioles (7.05 ± 2.20 μm)
revealed the highest frequencies (9.47 ± 2.89 cpm). Moreover, we reported that
nor-epinephrine and epinephrine increase the frequency of vasomotion, and vasomotion was reduced or abolished by isoproterenol, phentolamine, adenosine and
verapamil [9]. We observed, furthermore, that vasomotion frequencies changed at
arteriolar bifurcations [10]. These data indicate that all arterioles presented oscillations in diameter from the largest to the smallest, where branching points appeared
able to generate constriction and dilation of the vessels with complex overlapping
of waves regulating capillary blood flow. However, in [4] Bouskela and Grampp
reported data derived from hamster cheek pouch where they did not find any relationship between diameters and frequencies, with different changes in diameter (2–
10 μm) and frequencies in the range 3–15 cpm. In this case, arteriolar vasomotion
appeared as irregular vasomotor phenomenon difficult to explain. We could suggest
that surgical trauma and anesthesia might have influenced vasomotion patterns. In
our hamster cheek pouch preparations we did not observe regular vasomotion [11],
otherwise detected in unanesthetized hamster window preparation. In this preparation we investigated the changes in arteriolar vasomotion induced by anesthesia
and we observed disappearance of the arteriolar rhythmic diameter changes. After a
while there was a recovery of arteriolar vasomotion in alpha-chloralose anesthetized
animals [8]. However, improvements in methods of signal processing allowed us
to identify all frequency components in long-lasting recordings of pial arterioles in
anesthetized rats [19].
More recently, there have been several reports on vasomotion, especially in mesenteric arterioles, and the molecular mechanisms involved [1, 24], indicating that ion
fluxes are able to induce vasomotion and suggesting which mechanisms are operative
in vascular smooth muscle cells (a review of these mechanistic areas is beyond the
scope of this chapter and is dealt with elsewhere: see Chap. 20).
We investigated the changes in arteriolar vasomotion frequency and amplitude
in hamster skin fold chamber window preparation under hypoxia and hyperoxia,
reporting different responses between larger and smaller arterioles [2]. Hypoxia (8,
11 and 15% oxygen gas mixture inspiration), indeed, caused an increase in vasomotion frequency, a decrease in mean diameter and in capillary blood flow. These
effects were more pronounced with 8 and 11% oxygen gas mixture: high frequency
vasomotion shifted from order 1 and 2 to order 3 arterioles (24 ± 4 cpm, 11%
oxygen gas mixture). Hyperoxia (100% oxygen gas mixture) induced constriction of
the smallest vessels (order 1 and 2), decrease in mean diameter and in vasomotion
frequency, while order 3 arterioles dilated.
Improving our model, we implemented the hamster skin fold window preparation
to investigate the microvascular networks in the hamster skeletal muscle (Cutaneous
Maximus) [20]. We characterized the micro-arrangement of arterioles feeding the
muscle, where we found arterio-arteriolar anastomoses, called arcade arterioles, just
overlapping the layer of the skeletal muscle cells, from where originated the arterioles
penetrating among the muscle cells and feeding the skeletal tissue. Therefore, it is
reasonable to suggest that a blood reservoir (arcading system) is operative to feed
blood to cells according to their metabolic requirements. The terminal branching
275
related to arteriolar diameter, because the smallest arterioles (7.05 ± 2.20 μm)
revealed the highest frequencies (9.47 ± 2.89 cpm). Moreover, we reported that
nor-epinephrine and epinephrine increase the frequency of vasomotion, and vasomotion was reduced or abolished by isoproterenol, phentolamine, adenosine and
verapamil [9]. We observed, furthermore, that vasomotion frequencies changed at
arteriolar bifurcations [10]. These data indicate that all arterioles presented oscillations in diameter from the largest to the smallest, where branching points appeared
able to generate constriction and dilation of the vessels with complex overlapping
of waves regulating capillary blood flow. However, in [4] Bouskela and Grampp
reported data derived from hamster cheek pouch where they did not find any relationship between diameters and frequencies, with different changes in diameter (2–
10 μm) and frequencies in the range 3–15 cpm. In this case, arteriolar vasomotion
appeared as irregular vasomotor phenomenon difficult to explain. We could suggest
that surgical trauma and anesthesia might have influenced vasomotion patterns. In
our hamster cheek pouch preparations we did not observe regular vasomotion [11],
otherwise detected in unanesthetized hamster window preparation. In this preparation we investigated the changes in arteriolar vasomotion induced by anesthesia
and we observed disappearance of the arteriolar rhythmic diameter changes. After a
while there was a recovery of arteriolar vasomotion in alpha-chloralose anesthetized
animals [8]. However, improvements in methods of signal processing allowed us
to identify all frequency components in long-lasting recordings of pial arterioles in
anesthetized rats [19].
More recently, there have been several reports on vasomotion, especially in mesenteric arterioles, and the molecular mechanisms involved [1, 24], indicating that ion
fluxes are able to induce vasomotion and suggesting which mechanisms are operative
in vascular smooth muscle cells (a review of these mechanistic areas is beyond the
scope of this chapter and is dealt with elsewhere: see Chap. 20).
We investigated the changes in arteriolar vasomotion frequency and amplitude
in hamster skin fold chamber window preparation under hypoxia and hyperoxia,
reporting different responses between larger and smaller arterioles [2]. Hypoxia (8,
11 and 15% oxygen gas mixture inspiration), indeed, caused an increase in vasomotion frequency, a decrease in mean diameter and in capillary blood flow. These
effects were more pronounced with 8 and 11% oxygen gas mixture: high frequency
vasomotion shifted from order 1 and 2 to order 3 arterioles (24 ± 4 cpm, 11%
oxygen gas mixture). Hyperoxia (100% oxygen gas mixture) induced constriction of
the smallest vessels (order 1 and 2), decrease in mean diameter and in vasomotion
frequency, while order 3 arterioles dilated.
Improving our model, we implemented the hamster skin fold window preparation
to investigate the microvascular networks in the hamster skeletal muscle (Cutaneous
Maximus) [20]. We characterized the micro-arrangement of arterioles feeding the
muscle, where we found arterio-arteriolar anastomoses, called arcade arterioles, just
overlapping the layer of the skeletal muscle cells, from where originated the arterioles
penetrating among the muscle cells and feeding the skeletal tissue. Therefore, it is
reasonable to suggest that a blood reservoir (arcading system) is operative to feed
blood to cells according to their metabolic requirements. The terminal branching