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Departments of 1 Neuroscience and 2 Otolaryngology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Previous studies demonstrated that responses of a particular sympathetic nerve to vestibular stimulation depend on the type of tissue the nerve innervates as well as its anatomic location. In the present study, we sought to determine whether such precise patterning of vestibulosympathetic reflexes could lead to specific hemodynamic alterations in response to vestibular afferent activation. We simultaneously measured changes in systemic blood pressure and blood flow (with the use of Doppler flowmetry) to the hindlimb (femoral artery), forelimb (brachial artery), and kidney (renal artery) in chloralose-urethane-anesthetized, baroreceptor-denervated cats. Electrical vestibular stimulation led to depressor responses, 8 ± 2 mmHg (mean ± SE) in magnitude, that were accompanied by decreases in femoral vasoconstriction (23 ± 4% decrease in vascular resistance or 36 ± 7% increase in vascular conductance) and increases in brachial vascular tone (resistance increase of 10 ± 6% and conductance decrease of 11 ± 4%). Relatively small changes (<5%) in renal vascular tone were observed. In contrast, electrical stimulation of muscle and cutaneous afferents produced pressor responses (20 ± 6 mmHg) that were accompanied by vasoconstriction in all three beds. These data suggest that vestibular inputs lead to a complex pattern of cardiovascular changes that is distinct from that which occurs in response to activation of other types of somatic afferents.
blood flow; vascular resistance; vascular conductance; sympathetic nervous system
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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RECENT WORK DEMONSTRATED that activation of vestibular afferents leads to specific patterning of vestibulosympathetic reflexes (VSR) (10-12, 20). It has been suggested that activity of vasoconstrictor sympathetic efferents is preferentially influenced by electrical activation of vestibular afferents (11). As discussed in the previous paper (12), the responses of vasoconstrictor efferents to electrical vestibular stimulation are not homogeneous but depend on their innervation targets as well as their anatomic location. These findings suggest that the vestibular system has the potential to alter the tone of vascular beds located throughout the body. However, it is likely that these changes are not uniform but instead are patterned and lead to specific hemodynamic alterations. The goal of the present study was to determine whether electrical vestibular stimulation leads to patterned changes of regional vascular tone. In particular, this investigation had three specific objectives. The first aim was to determine whether changes in vascular resistance and conductance elicited by vestibular stimulation are greater in the limbs or in the kidney. The second aim was to establish whether there is a difference between forelimb and hindlimb vascular resistance changes to vestibular stimulation, as would be predicted by a previous observation that VSR recorded from forelimb and hindlimb vasoconstrictor fibers are qualitatively different (12). The third aim was to determine whether regional vascular resistances are affected in a similar manner by vestibular signals as by inputs from muscle and skin. To address these aims, systemic blood pressure and blood flow to the hindlimb, forelimb, and kidney were simultaneously measured during stimulation of either the vestibular nerve or limb nerves containing skin and muscle afferents.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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All the procedures used in this study conformed to the American Physiological Society's Guiding Principles for the Care and Use of Animals and were approved by the University of Pittsburgh's Animal Care and Use Committee.
Surgical procedures.
Experiments were performed on nine adult cats weighing between 3.3 and
5.1 kg (supplied by Liberty Laboratories, Waverley, NY). Animals were
premedicated with a mixture of ketamine (15-20 mg/kg im) and
xylazine (0.1-0.2 mg/kg im) and were then anesthetized with a
mixture of 
-chloralose (40 mg/kg iv) and urethane (200 mg/kg
iv). The depth of anesthesia was determined as adequate if
withdrawal reflexes to noxious stimuli were absent and the pupils
remained constricted. Chloralose-urethane supplements (~10% of the
initial dose) were administered as necessary to maintain this level of anesthesia.
Data recording procedures. Blood flow cuffs were connected to a directional pulsed Doppler flowmeter (model 545C, University of Iowa Bioengineering, Iowa City, IA). Doppler frequency shift (in kHz) in blood flow velocity as measured by the flowmeter correlates well with regional blood flow changes (5). The range of the blood flow transducer was adjusted so that the strongest phasic signal from each flow cuff was recorded (see Fig. 1A for examples). Afterward, the mean flow signal was sampled from the mean output port of the flowmeter. Mean blood flow and pulsatile blood pressure signals were digitized at 100 Hz (with the use of a model 1401-plus analog-to-digital converter, Cambridge Electronic Design, Cambridge, UK) and fed into a computer (Macintosh Quadra 800) to allow continuous online measurement. Data sampling and subsequent analyses were performed with the use of Spike2 software (Cambridge Electronic Design). Mean arterial pressure was determined over 1-s bins; heart rate was also calculated over 1-s intervals on the basis of the average interval between systolic blood pressure peaks. To determine whether changes in blood flow were due to active constriction or relaxation of local vasculature (as opposed to passive changes in flow resulting from systemic blood pressure alterations), resistance was calculated off-line by dividing blood pressure (in mmHg) by the Doppler shift (kHz) of the blood flow velocity signal for each vascular bed. To ensure that possible changes in baseline flow rates did not bias our conclusions regarding changes in local vascular tone (18), conductance was also calculated by dividing the blood flow velocity signal by blood pressure. Resistance and conductance measurements were expressed as percent change from mean control values (taken during the 10- or 20-s period immediately preceding stimulation onset).
Stimulation procedures. To elicit cardiovascular responses, vestibular afferents on one side were activated with stimulus trains of square-wave shocks (0.2-ms pulse duration, 333-Hz stimulus frequency, 30- to 40-s train duration) repeated every 2-5 min. Responses of up to 15 stimulus repetitions were recorded and averaged. In seven cats, stimulation intensity was set just below the facial movement threshold at 470 ± 92 µA (mean ± SE), which was 3.3 ± 0.4 times the threshold for eliciting eye movements. In three animals, lower intensity stimuli were also shown to elicit cardiovascular responses that were qualitatively similar, although smaller in magnitude than those elicited by stimuli that were just below facial nerve threshold. In one animal, eye and facial movements were not measured, and in another cat eye movements could not be elicited, presumably due to the depth of anesthesia. In the latter animal, activation of vestibular afferents was confirmed by recording field potentials from the ipsilateral vestibular nuclei. In both of these animals, the intensity of vestibular stimulation was set to 500 µA, a value that was close to mean intensity of vestibular stimulation used in the other animals.
Skin and muscle afferents in the ulnar or median nerve were activated with the use of similar stimulus parameters as those employed to elicit vestibulocardiovascular responses. Stimulus intensity ranged from 3 to 10 mA but was set at a constant level within each experiment. We previously determined that stimulation intensities in this range lead to maximal sympathetic nerve responses (10) and therefore would likely produce maximal cardiovascular changes.Statistical methods. Differences in response sizes and response latencies were evaluated with the use of a one-way ANOVA (InStat 1.12 for Macintosh). Post hoc statistical testing was performed with the use of the Bonferroni multiple comparisons test. Significance was set at P < 0.05. Pooled data are presented as means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Electrical stimulation of vestibular afferents led to depressor
responses in all nine animals (see Fig.
1B for an example), whose
baseline blood pressure was 116 ± 5 mmHg and baseline heart rate
was 253 ± 11 beats/min. The magnitude of the depressor response elicited by the maximal stimulus intensity employed in each experiment ranged from 2 to 16 mmHg (Table 1); the
mean decrease in blood pressure was 8 ± 2 mmHg. Lower stimulus
intensities elicited qualitatively similar, although smaller, decreases
in blood pressure. The latency of peak depressor responses was
13.7 ± 9.0 s. In five of the animals, these peak depressor
effects were accompanied by decreases in heart rate of 2-9
beats/min (latency of 12.0 ± 7.5 s; Fig. 1B), whereas no heart rate changes were observed in the other animals. The
mean decrease in heart rate elicited by vestibular stimulation in all
animals was 3 ± 1 beats/min.
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Changes in blood pressure elicited by vestibular stimulation were
typically accompanied by increases in blood flow to femoral vasculature, decreases in blood flow to brachial vasculature, and
relatively small changes in renal arterial blood flow (Fig. 1B). Examples of vascular resistance changes elicited by
vestibular stimulation are illustrated in Fig.
2. Resistance changes occurred within a
few seconds and reached their maximum 10-25 s after the onset of
vestibular stimulation. The mean latencies of peak responses were
14.6 ± 2.5, 18.3 ± 4.2, and 16.0 ± 3.3 s for
femoral vascular resistance (FVR), brachial vascular resistance (BVR),
and renal vascular resistance (RVR), respectively. The differences in
response latencies were not statistically significant
(P > 0.05, ANOVA). The response patterns were similar
across the range of stimulus intensities used in this study (which were
subthreshold for producing current spread to nonvestibular
afferents), although in some cases the threshold for producing a
detectable change in resistance in a particular vascular bed was
slightly lower than for others (e.g., see Fig. 2C).
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Maximal changes in vascular resistance and conductance were calculated in each animal and are presented in Table 1. In five cats (animals 1-5 in Table 1), vestibular stimulation elicited decreases in FVR of 15-37% in magnitude, whereas BVR increased by 7-44%. Changes in flow in one of these cats (animal 5) are illustrated in Fig. 1B. In three of these animals, relatively small decreases (3-10%) in RVR were observed, whereas in two other animals, increases of ~3% in RVR were measured. However, in two animals (animals 6 and 7 in Table 1), vestibular stimulation produced either a selective increase in BVR or a selective decrease in FVR, whereas little change in resistance occurred in the other vascular beds. In one of these animals, BVR increased by 17%, whereas only a 2% change in FVR was observed. In the other animal, FVR decreased by 44%, whereas BVR showed a relatively small decrease of 9%. In both of these animals, relatively small changes in RVR were observed. Only in one cat (animal 8 in Table 1) were qualitatively and quantitatively similar changes in FVR, BVR, and RVR observed. In the remaining cat (animal 9 in Table 1), vestibular stimulation led to a selective decrease in FVR of 20%, whereas no change in RVR was observed. Brachial artery flow was not measured in this cat. Changes in conductance during vestibular stimulation typically paralleled the changes in vascular resistance, reflecting decreased vascular tone in the femoral vasculature, increased vascular tone in the brachial vascular bed, and little alteration in the tone of the renal vasculature.
Overall, FVR decreased and femoral vascular conductance (FVC) increased
in eight of nine animals. The average maximal decrease in resistance in
response to vestibular stimulation was 23 ± 4% in all animals,
whereas conductance increased by 36 ± 7% (Fig. 3). BVR increased in six and decreased in
two of eight animals, whereas brachial vascular conductance (BVC)
decreased in seven of eight animals. The mean maximal BVR increase for
all animals was 10 ± 6%, and the mean decrease in maximal BVC
was 11 ± 4% (Fig. 3). RVR decreased in five of nine animals,
whereas only small (<3%) changes were observed in the other animals,
and similar but reciprocal alterations in renal vascular conductance
(RVC) were also noted. RVR decreased by 4 ± 2% across all of the
animals, whereas RVC increased by only 2 ± 2% (Fig. 3). Both
resistance and conductance changes elicited by vestibular stimulation
in the renal, brachial, and femoral vascular beds were significantly different (P < 0.001, ANOVA). Post hoc statistical
testing confirmed that differences between FVR and RVR as well as
between FVC and RVC were statistically significant (P < 0.05, Bonferroni test). Likewise, differences between FVR and BVR
and between FVC and BVC were also significant (P < 0.05). Differences in changes of RVR and BVR exhibited a trend toward
significance (uncorrected P = 0.05) as did the
difference between RVC and BVC (uncorrected P = 0.08).
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To determine whether observed changes in regional hemodynamics were
specific to vestibular stimuli, we also examined resistance and
conductance changes produced by activation of skin and muscle afferents. These responses were studied in the same animals that were
used for determination of hemodynamic alterations elicited by
vestibular stimulation. Muscle and cutaneous afferents were activated
by delivering a high-intensity electrical stimulus to the right ulnar
(8 cats) or the right median (1 cat) nerve. In response to these
stimuli, blood pressure increased by 20 ± 6 mmHg (11.4 ± 1.8-s latency), whereas heart rate increased by 7 ± 2 beats/min
(14.5 ± 1.8-s latency; see Fig. 4
for examples of responses). These changes were accompanied by
alterations in vascular resistance and conductance in all of the
animals that peaked within 5-15 s of stimulus onset (Fig. 4).
Overall, the latencies of peak increases in vascular resistance
elicited by limb nerve stimulation were 11.0 ± 1.8, 9.1 ± 1.4, and 14.6 ± 2.4 s for FVR, BVR, and RVR, respectively;
these differences did not reach statistical significance
(P > 0.05, ANOVA).
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Limb nerve stimulation elicited a marked increase in FVR and a large
decrease in FVC in all of the animals. However, in two cases, the flow
signal decreased to zero during stimulus periods, likely due to strong
vasoconstriction, and recovered after each stimulus. This decrease in
flow saturated resistance measurements and prevented us from accurate
quantification of this parameter. In the other animals, the magnitude
of changes in FVR ranged from 28 to 1,120%, whereas FVC decreased by
24-90%. Changes in BVR and BVC during limb nerve stimulation were
qualitatively similar to those in FVR and FVC, respectively. These
parameters were measured in every animal; the increase in BVR ranged
from 18 to 200%, whereas the decrease in BVC ranged from 15 to 59%.
RVR increased by 8-78% in six of the animals and decreased by
10% in another. In two of the animals, no appreciable changes in renal
artery resistance were observed during limb nerve stimulation.
Similarly, RVC decreased by 12-46% in four animals, increased by
8-11% in two animals, and was relatively unaffected (change 
4%) in three animals.
Overall, simultaneous activation of skin and muscle afferents led to
increases of 406 ± 155 and 62 ± 23% for FVR and BVR, respectively (Fig. 5). The mean change in
RVR was 17 ± 9% (Fig. 5). The differences in the magnitude of
these peak resistance changes were statistically significant
(P < 0.001, ANOVA). Post hoc statistical analysis
confirmed that differences between changes in FVR and BVR as well as
those between FVR and RVR were significant (P < 0.05, Bonferroni test). The differences in magnitude of changes between RVR
and BVR did not reach statistical significance (P > 0.05). Similarly, limb nerve stimulation elicited decreases in FVC,
BVC, and RVC of 70 ± 7, 31 ± 6, and 10 ± 6%,
respectively (Fig. 5). These differences in mean peak conductances were
statistically significant (P < 0.05, ANOVA), and post
hoc statistical analysis confirmed that differences between changes in
FVC and BVC as well as those between FVC and RVC were significant
(P < 0.05, Bonferroni test), whereas those between RVC
and BVC were not (P > 0.05).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The major new finding of the present study is that vestibular stimulation has the potential to produce patterned hemodynamic alterations that preferentially affect the limb vasculature as opposed to that of the kidney. Additionally, in many animals, changes in hindlimb and forelimb vascular resistance and conductance elicited by electrical vestibular stimulation are qualitatively different such that the hindlimb resistance decreases (and conductance increases), whereas the forelimb resistance increases (and conductance decreases). In contrast, activation of skin and muscle afferents produces a different pattern of hemodynamic responses that includes a parallel increase in forelimb and hindlimb vascular resistance (or a decrease in conductance) in the three vascular beds. Although a previous study showed that stimulation of the A5 area of the brain stem can produce changes in blood flow to muscles in some parts of the body but not others (23), the present data indicate that inputs from a particular sensory system (the vestibular system) can also elicit patterned hemodynamic responses.
One caveat in our data analysis is that we calculated vascular resistance and conductance from measurements of blood pressure and Doppler frequency shift in blood flow velocity. These calculations rely on the assumption that venous pressure does not change independent of arterial blood flow. Because we did not measure venous pressure in this study, we are uncertain that this assumption is completely valid. Nonetheless, it seems highly unlikely that in the paralyzed animals used in this study changes in venous pressure could account for the patterning of blood flow that was observed during vestibular stimulation. Another limitation in these experiments is that blood flow to the muscle and skin could not be distinguished, so that reciprocal changes in blood flow to the muscle and skin of a limb would appear as the absence of a local hemodynamic alteration. Follow-up studies will be required to determine whether electrical vestibular stimulation alters blood flow to the muscle, skin, or to both tissues.
Other investigators have reported that unilateral electrical vestibular stimulation produces blood pressure decreases of >20 mmHg in baroreceptor-intact cats (7, 16, 25), whereas bilateral vestibular stimuli produce even larger decreases in blood pressure (6). In the present study, vestibular-elicited depressor responses were considerably smaller in magnitude (~8 mmHg), although qualitatively similar to those reported earlier (6). Several factors may have accounted for smaller response sizes in this study. First, we limited the current intensities applied to the vestibular nerve to assure that nonlabyrinthine afferents were not activated; it is likely that larger stimuli would have produced greater changes in blood pressure. The anesthetic regimen employed in these experiments as well as the frequency of vestibular stimulation delivered could also have diminished response sizes. Presumably, different parameters of vestibular stimulation delivered in unanesthetized animals would produce larger changes in vascular resistance than were observed in this investigation. Additionally, it is feasible that vestibular inputs act on the baroreceptor reflex circuitry to produce cardiovascular responses. Such is the case with inputs that are activated as part of the autonomic response of the defense reaction (22). It is therefore possible that larger cardiovascular changes would be observed in baroreceptor-intact cats than were elicited in the present experiments.
In the companion manuscript, we reported anatomic differences in responses of muscle vasoconstrictor sympathetic efferents to electrical vestibular stimulation (12). Specifically, activity of single muscle vasoconstrictor efferents located in the hindlimb was typically initially inhibited by vestibular stimulation; these inhibitory responses were typically followed by "rebound" excitation. In contrast, responses of muscle vasoconstrictor units located more rostrally (in the head and forelimb) often included a short duration excitatory phase that preceded the inhibition. In the present study, we found that vascular resistance changes elicited by vestibular stimulation parallel the shortest latency responses of muscle vasoconstrictor fibers. It is thus tempting to speculate that the observed hemodynamic effects reflected sympathetically mediated changes in blood flow to muscle but not to skin. However, it cannot be ruled out that activation of sympathetic vasodilator fibers in the hindlimb as well as liberation of adrenal catecholamines contributed to the responses observed in the present study.
The small magnitude of changes in RVR and RVC elicited by vestibular stimulation suggests that this vascular bed is relatively unresponsive (as compared with the hindlimb) to labyrinthine inputs. This finding is somewhat surprising given the fact that renal nerve activity is much more powerfully affected by vestibular stimulation than that of other visceral sympathetic nerves that have been examined (11). One reason for this discrepancy may be differences between the characteristics of vestibular stimulation used in the present study and in the previous experiment in which sympathetic nerve activity was recorded. In the nerve recording study, responses to 200-400 brief (15 ms) stimulus trains repeated every 1-2 s were averaged (11). In the present study, stimulus trains were much longer, were repeated fewer times, and were separated by longer periods. It is feasible that the former parameters of vestibular stimulation would elicit more pronounced changes in vasoconstrictor activity than would the latter. An alternative possibility is that sympathetic nerve responses and those of vascular smooth muscle are dissociated in the kidney during vestibular stimulation. Several lines of evidence suggest that renal blood flow can remain constant during increases or decreases in renal sympathetic nerve activity. For example, occlusion of the common carotid arteries leads to a large increase in renal sympathetic nerve activity (19), but it fails to appreciably change renal blood flow (4, 13). Likewise, other baroreceptor stimuli (such as loading or unloading of the atrial stretch receptors) produce little or no change in blood flow to the kidney (4), although renal sympathetic nerve activity is altered markedly (11, 19). In contrast, stimuli such as hypoxia and those that lead to alerting and defensive behaviors produce considerable sympathetically mediated renal blood flow alterations (3, 9, 14). Further experiments will be required to determine the functional significance of vestibular effects on sympathetic outflow to the kidney.
Electrical stimulation was used to activate vestibular afferents in this study, as this method powerfully and selectively elicits vestibular inputs to the central nervous system. Many previous studies (e.g., 7, 16, 24, 25) have examined the effects of electrical vestibular stimulation on blood pressure and have shown that this method elicits depressor responses. In contrast, stimulation of a subset of vestibular afferents (in decerebrate, unanesthetized cats) signaling a head-up movement produces pressor responses (27). Thus the results of this study cannot be used to conclusively predict the pattern of hemodynamic changes that would be elicited by a particular direction of movement. Nonetheless, because stimulation of the whole vestibular nerve produces patterned hemodynamic responses, it seems likely that selective activation of subsets of vestibular afferents (either through body movements in space or electrical stimulation of individual branches of the vestibular nerve) would also generate patterned changes in blood flow to different tissues and body regions. Because vestibular afferents are activated during the act of falling in the cat (26), it is possible that electrical stimulation of the whole vestibular nerve elicits a hemodynamic response that would typically be associated with vestibulospinal reflexes during such body translations in space. These responses could require an increase in blood flow to the large hindlimb muscles that the animal predominantly uses to "catch" itself after a fall. However, stimulation of the subset of vestibular afferents that would be activated during nose-up body rotations may produce a different pattern of blood flow in the body that is appropriate to offset an orthostatic challenge.
In contrast to vestibular afferents, stimulation of limb nerves elicited an increase in resistance and a decrease in conductance in all three vascular beds that were studied, accompanied by tachycardia and blood pressure increases. These observations are consistent with findings from other studies (2, 8, 17), indicating that pressor responses accompanied by widespread sympathetically mediated vasoconstriction occur in response to electrical stimulation of somatic nerves in anesthetized cats and dogs. In an earlier study, we reported that the pattern of responses of visceral sympathetic nerves to vestibular stimulation is different from that elicited by activation of limb afferents (10). The current study extends those findings by demonstrating that differences in sympathetic nerve responses to stimulation of vestibular and other somatic afferents are also reflected in distinct cardiovascular responses, which may involve complicated redistributions of blood flow to different body regions.
Perspectives
The present study has demonstrated that electrical vestibular stimulation produces patterned alterations in the hemodynamics of limb vasculature, which include hindlimb vasodilation and forelimb vasoconstriction with relatively small changes in renal circulation. Taken together with the findings of the preceding paper, it is most likely that this reciprocal patterning is produced by withdrawal of sympathetic vasoconstrictor drive to the hindlimb muscle vasculature together with increased activity of forelimb muscle vasoconstrictor efferents. Because the vestibular system plays an important role in controlling motoneuron activity during unexpected postural changes (26), it is possible that the sympathetic patterning described in the present studies represents a complementary and preparatory autonomic response to motor activation that occurs during postural adjustments (e.g., righting). Accordingly, previous studies have suggested a role of the vasomotor sympathetic outflows for blood flow redistribution to muscle immediately before the onset of muscle contraction during willful dynamic exercise (1) or in response to emotional stimuli that produce fighting behavior (15). In addition, vestibular inputs may participate in eliciting regional changes in vascular tone to offset venous pooling during movements that challenge orthostatic stability (27). These possibilities will require further investigation with the use of more natural stimuli than were employed in the present experiments. Likewise, the integration of vestibular inputs with feedforward (i.e., central command) and feedback (i.e., afferent input from contracting muscles) mechanisms that regulate sympathetic activity during movement and exercise needs to be further explored.| |
ACKNOWLEDGEMENTS |
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We thank Drs. Alan Sved, Regis Vollmer, and Linda Rinaman for helpful comments on a previous version of this manuscript. We are also grateful to Dr. Alan Sved for providing the Doppler flowmeter used in these experiments and for guidance and advice regarding the use of this equipment. Lucy Cotter and David Eisenberg provided excellent technical assistance during the course of this work.
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FOOTNOTES |
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This study was supported by National Institutes of Health Grants R01-DC-00693, R01-DC-03732, and P01-DC-03417 to B. J. Yates. I. A. Kerman is supported by National Aeronautics and Space Administration Graduate Student Researcher's Program (fellowship GSRP 97-125).
Address for reprint requests and other correspondence: B. J. Yates, Dept. of Otolaryngology, Univ. of Pittsburgh, Eye and Ear Institute, 203 Lothrop St., Pittsburgh, PA 15213 (E-mail: byates{at}pitt.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Received 4 October 1999; accepted in final form 31 January 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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