17 Biological Oscillations of Vascular Origin and Their Meaning …
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“switch on and off” was effective in opening or closing the branching vessel, regulating the volume of blood perfusing the active skeletal muscle cells. The difference
between terminal order 4 and order 3 arterioles, branching from arcade arterioles,
was in the frequency rate, higher in order 3 than in order 4 vessels. Moreover, order 3
arterioles completely constricted during the vasomotion cycle, and this constriction
wave was conducted through the daughter arterioles up to the capillaries (usually
24 ± 9, for each terminal unit). Therefore, all the capillaries presented stop and go
blood flow, according to the activity of parent order 3 arteriole. The long terminal
trees, conversely, originated 45 ± 6 capillaries, where the stop and go mechanism
was asynchronous, due to the different points of activity in the daughter vessels
spreading from the parent order 4 arteriole. These features permit to increase the
blood volume supply to the tissue by 273 and 239% compared to the baseline, on the
average, for the short and long terminal trees, respectively. Therefore, it is reasonable
to suggest that frequency oscillations in the ranges 0.01–0.08 and 0.08–0.16 derive
from arteriolar vasomotion, i.e. from mechanisms regulating the blood flow distribution to the tissues. It is worth noting that larger arterioles are densely innervated and
their activity is largely influenced by sympathetic nervous system discharge, while
smaller arterioles are most influenced by features of smooth muscle cells endowed
in the arteriolar walls.
17.3 Vasomotion in Rat Closed Cranial Window
In another experimental preparation, the rat closed cranial window, under αchloralose anaesthesia, we recorded rhythmic diameter changes in pial arterioles
observed through the window localized on the left parietal cortex [19]. We recorded
the rhythmic changes for 30 min and processed the diameter changes with the
generalized short time Fourier transform (GSTFT) to evaluate the frequency components. We detected six components in the rhythmic diameter change recordings. Our
aim was to characterize each component; consequently, we used many substances
to stimulate or inhibit the endothelial or smooth muscle factors: acetylcholine,
papaverine, Nω-Nitro-L-arginine (L-NNA), inhibitor of eNOS; indomethacin
(INDO), inhibitor of prostaglandin endoperoxidase; charybdotoxin plus apamin,
inhibitors of endothelium-derived hyperpolarizing factor (EDHF). We observed that
under baseline conditions, the range of the first component was: 0.001–0.0095 Hz
(0.06–0.57 cpm); of the second: 0.0095–0.02 Hz (0.57–1.2 cpm); of the third: 0.02–
0.06 Hz (1.2–3.6 cpm); of the fourth: 0.06–0.2 Hz (3.6–12 cpm); of the fifth: 0.2–
2.0 Hz (12–120 cpm) and of the sixth: 2.0–4.5 Hz (120–270 cpm) (Table 17.1). The
sixth component had the highest power spectral density in order 2 and 3 arterioles
(mean diameter: 23.8 ± 1.4 μm and 33.5 ± 1.8 μm, respectively), followed by the
fourth, third, second and first component. In order 4 vessels (mean diameter: 43.7
±1.4) the sixth component showed the highest spectral density, but there was an
increase in the first and second components, while there was a decrease in third
and fifth components. Our data indicate that acetylcholine caused an increase in
277
“switch on and off” was effective in opening or closing the branching vessel, regulating the volume of blood perfusing the active skeletal muscle cells. The difference
between terminal order 4 and order 3 arterioles, branching from arcade arterioles,
was in the frequency rate, higher in order 3 than in order 4 vessels. Moreover, order 3
arterioles completely constricted during the vasomotion cycle, and this constriction
wave was conducted through the daughter arterioles up to the capillaries (usually
24 ± 9, for each terminal unit). Therefore, all the capillaries presented stop and go
blood flow, according to the activity of parent order 3 arteriole. The long terminal
trees, conversely, originated 45 ± 6 capillaries, where the stop and go mechanism
was asynchronous, due to the different points of activity in the daughter vessels
spreading from the parent order 4 arteriole. These features permit to increase the
blood volume supply to the tissue by 273 and 239% compared to the baseline, on the
average, for the short and long terminal trees, respectively. Therefore, it is reasonable
to suggest that frequency oscillations in the ranges 0.01–0.08 and 0.08–0.16 derive
from arteriolar vasomotion, i.e. from mechanisms regulating the blood flow distribution to the tissues. It is worth noting that larger arterioles are densely innervated and
their activity is largely influenced by sympathetic nervous system discharge, while
smaller arterioles are most influenced by features of smooth muscle cells endowed
in the arteriolar walls.
17.3 Vasomotion in Rat Closed Cranial Window
In another experimental preparation, the rat closed cranial window, under αchloralose anaesthesia, we recorded rhythmic diameter changes in pial arterioles
observed through the window localized on the left parietal cortex [19]. We recorded
the rhythmic changes for 30 min and processed the diameter changes with the
generalized short time Fourier transform (GSTFT) to evaluate the frequency components. We detected six components in the rhythmic diameter change recordings. Our
aim was to characterize each component; consequently, we used many substances
to stimulate or inhibit the endothelial or smooth muscle factors: acetylcholine,
papaverine, Nω-Nitro-L-arginine (L-NNA), inhibitor of eNOS; indomethacin
(INDO), inhibitor of prostaglandin endoperoxidase; charybdotoxin plus apamin,
inhibitors of endothelium-derived hyperpolarizing factor (EDHF). We observed that
under baseline conditions, the range of the first component was: 0.001–0.0095 Hz
(0.06–0.57 cpm); of the second: 0.0095–0.02 Hz (0.57–1.2 cpm); of the third: 0.02–
0.06 Hz (1.2–3.6 cpm); of the fourth: 0.06–0.2 Hz (3.6–12 cpm); of the fifth: 0.2–
2.0 Hz (12–120 cpm) and of the sixth: 2.0–4.5 Hz (120–270 cpm) (Table 17.1). The
sixth component had the highest power spectral density in order 2 and 3 arterioles
(mean diameter: 23.8 ± 1.4 μm and 33.5 ± 1.8 μm, respectively), followed by the
fourth, third, second and first component. In order 4 vessels (mean diameter: 43.7
±1.4) the sixth component showed the highest spectral density, but there was an
increase in the first and second components, while there was a decrease in third
and fifth components. Our data indicate that acetylcholine caused an increase in