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-Adrenergic vasoconstriction in active skeletal muscles
during dynamic exercise
Departments of Anesthesiology and Physiology, Medical College of Wisconsin and Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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Sympathetic vasoconstriction in working muscles
during dynamic exercise has been demonstrated by intra-arterial
administration of 
1-adrenergic
antagonists. The purpose of this study was to examine the existence of
1- and
2-adrenergic receptor-mediated vasoconstriction in active skeletal muscles during
exercise. Six mongrel dogs were instrumented chronically
with flow probes on the external iliac arteries of both hindlimbs, and
a catheter was inserted in one femoral artery. All dogs ran on a
motorized treadmill at three exercise intensities (3 miles/h, 6 miles/h, and 6 miles/h at 10% grade) on separate days. After 5 min of
exercise, a selective 1-
(prazosin) or a selective
2-adrenergic antagonist (rauwolscine) was infused as a bolus into the femoral arterial catheter
(only one drug per day). The doses of the antagonists were adjusted to
maintain the same effective concentration at each exercise intensity.
At the mild, moderate, and heavy workloads prazosin infusion produced
immediate increases in iliac conductance of 65 ± 9, 35 ± 6, and 18 ± 4% (means ± SE), respectively, and increases in blood flow of
290 ± 24, 216 ± 23, and 172 ± 18 ml/min, respectively. Rauwolscine infusion produced increases in
conductance of 52 ± 5%, 36 ± 5%, and 26 ± 3%,
respectively, and blood flow increases of 250 ± 34, 244 ± 39, and 259 ± 35 ml/min at the three workloads. Systemic
blood pressure and blood flow in the contralateral iliac artery were
unaffected by any of the antagonist infusions. These results
demonstrate that there is ongoing
1- and
2-adrenergic receptor-mediated
vasoconstriction in exercising skeletal muscles even at heavy workloads
and that the magnitude of vasoconstriction decreases as exercise
intensity increases.
blood flow; sympathetic nervous system; 2-adrenergic receptor; rauwolscine; dogs
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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AT THE ONSET OF EXERCISE there is an increase in
sympathetic nerve activity to inactive tissues (25) and active skeletal muscle (6). This increase in sympathetic outflow directs blood flow
away from inactive tissue and is essential to the maintenance of
elevated blood pressure during exercise, i.e., the exercise pressor
response (5). As exercise intensity increases, a greater proportion of
cardiac output is directed toward active skeletal muscle. It has been
argued that this makes active skeletal muscle an increasingly important
site for sympathetic vasoconstriction to regulate blood pressure (32).
However, a number of studies (30, 31, 37) reported a decreased
vasoconstrictor response to sympathetic activation in contracting
skeletal muscle ("sympatholysis"). A completely abolished
constrictor response in active skeletal muscle is unlikely because
there is strong evidence for tonic sympathetic vasoconstriction in
active skeletal muscle (2, 14, 28). Using intra-arterial infusion of a
selective 1-adrenergic antagonist, Buckwalter et al. (2) and O'Leary et al. (28) clearly
demonstrated that there is tonic
1-adrenergic receptor-mediated vasoconstriction in the hindlimb vasculature of dogs running on a
treadmill. However, these studies drew opposite conclusions regarding
the magnitude of the sympathetic restraint of blood flow in active
skeletal muscle as it relates to exercise intensity. Neither of these
studies attempted to examine the existence of 2-adrenergic receptor-mediated
vasoconstriction in active skeletal muscle.
Although 2-adrenergic receptors
were originally believed to be located only on the presynaptic nerve
terminal, subsequent studies demonstrated the existence of postsynaptic
2-receptors in vascular smooth
muscle (8). It is generally accepted that both
1- and
2-adrenergic receptors (as well
as various subtypes) exist in various sites of the vasculature (4, 34).
Postsynaptic 2-adrenergic
receptors contribute to the neurally mediated tone in the skeletal
muscle vasculature of the anesthetized dog (11, 16). Furthermore,
vasoconstrictor responses to sympathetic stimulation (10) and
norepinephrine infusion (10, 13) are mediated by both
1- and
2-adrenergic receptors. The
effect of selective blockade of
2-adrenergic receptors on blood
flow to active skeletal muscle during exercise has not been examined.
The purpose of this study was to examine the existence of tonic
2-adrenergic receptor-mediated
vasoconstriction to active skeletal muscle in a conscious animal during
dynamic exercise. Second, we examined the relationship between tonic
-adrenergic receptor-mediated vasoconstriction in active skeletal
muscle and exercise intensity. We hypothesized that there
is both 1- and 2-adrenergic receptor-mediated
restraint of blood flow in exercising skeletal muscle. In addition, we
hypothesized that the magnitude of -adrenergic vasoconstriction in
active skeletal muscle is inversely related to exercise intensity.
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METHODS AND PROCEDURES |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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All experimental procedures were approved by the Institutional Animal Care and Use Committee and conducted in accordance with the American Physiological Society's "Guiding Principles in the Care and Use of Animals." Mongrel dogs (n = 6, 21.3 ± 0.21 kg) were selected for their willingness to run on a motorized treadmill and were chronically instrumented using sterile surgical procedures. Anesthesia was induced with thiopental sodium (15-30 mg/kg; Gensia Pharmaceuticals, Irvine, CA) and maintained by mechanical ventilation with 1.5% halothane (Halocarbon Laboratories, River Edge, NJ) and 98.5% oxygen after intubation with a cuffed endotracheal tube. Antibiotic (cefazolin sodium, Apothecon, Princeton, NJ) and analgesic drugs (buprenorphine hydrochloride, 0.3 mg; Reckitt and Colman, Kingston-Upon-Hull, UK) were given postoperatively. During the first surgical procedure, the carotid arteries were surgically exteriorized so that they could be cannulated percutaneously to measure arterial blood pressure (23, 24). In the second surgery, the dogs were instrumented with 4-mm ultrasonic transit time flow probes (Transonic Systems, Ithaca, NY) around the external iliac arteries to provide measurements of hindlimb blood flow. The cables were tunneled under the skin to the back, and the dogs were given 2 wk to recover. In the final surgery, a heparinized catheter for drug infusion (0.045-in. OD, 0.015-in. ID, 60-cm length, Data Science International, St. Paul, MN) was implanted through a side branch into the femoral artery, and the free end was tunneled to the back of the dog. To maintain patency, the catheter was flushed daily with saline and filled with a heparin lock (100 IU heparin/ml in 50% dextrose solution). The dogs were given at least 2 days to recover from the final surgery before any experiments were performed.
On each experimental day the dog was brought to the laboratory, which
was maintained at a temperature below 20°C. A 20-gauge catheter
(Insyte, Becton-Dickinson, Sandy, UT) was inserted retrogradely into
the lumen of the carotid artery and attached to a solid-state pressure
transducer (Ohmeda, Madison, WI). The dogs were placed on a motorized
treadmill (Quinton Instruments, Seattle, WA), and the flow probes were
connected to a transit time flowmeter (Transonic Systems). On separate
days, the dogs ran at three different intensities: 3 miles/h (4.8 km/h)
0% grade, 6 miles/h (9.7 km/h) 0% grade, or 6 miles/h (9.7 km/h) 10%
grade. Prazosin, a selective
1-antagonist (Pfizer, Groton,
CT), was dissolved in propylene glycol and diluted with sterile water
to a concentration of 200 µg/ml. Rauwolscine, a selective
2-antagonist (RBI, Natick, MA),
was dissolved in sterile water to a concentration of 2 mg/ml. Both of
these antagonists have been previously shown to be effective at
producing selective -adrenergic blockade in skeletal muscle (1, 9).
The dogs ran on the treadmill at 3 miles/h. At 5 min of exercise, a
bolus of antagonist (50 µg prazosin or 1 mg rauwolscine) was infused into one femoral artery. Antagonist infusions were given at the same
time point at the two higher exercise intensities. The dose of the
antagonist was proportionally adjusted to account for the exercise
intensity-induced increases in iliac blood flow (drug dose = 3 miles
per hour drug dose × exercise blood flow/3 miles per hour blood
flow). The doses of the selective -adrenergic receptor antagonists
used in this study were chosen because of their ability to abolish the
substantial vasoconstriction induced by 10 µg of the
1-selective agonist
phenylephrine and 10 µg of the
2-selective agonist clonidine,
respectively. In each experiment, the selective -adrenergic receptor
antagonist completely abolished the effect of the appropriate agonist.
All experiments were performed in duplicate, and the data were averaged
for each dog. Only one bout of exercise and one receptor antagonist
were examined per day (36 separate experiments on 36 separate days).
Intra-arterial infusions of the solvent vehicle have previously been
shown not to affect iliac blood flow (2, 3).
Arterial blood pressure and right and left external iliac blood flow were written simultaneously to paper on a polygraph recorder (Grass, Quincy, MA) and stored on both a video cassette data recorder (Vetter, Rebersburg, PA) and computer (Apple 8500 Power PC) using a MacLab system at 100 Hz (ADInstruments, Castle Hill, Australia). Data were analyzed off-line using the MacLab software to calculate mean arterial pressure, heart rate, iliac blood flow, and iliac vascular conductance (blood flow/mean arterial pressure). Control measurements were averaged over 30 s before the antagonist infusion. After the antagonist infusion, all variables were averaged over 1-s intervals, and the highest 1-s average was chosen as the peak response. Statistical analyses of heart rate, mean arterial blood pressure, blood flow, and conductance were performed with a two-way (drug × exercise intensity) repeated-measures analysis of variance. The percent changes from baseline in conductance after the infusion of the antagonists were analyzed with a one-way repeated-measures analysis of variance. Where significant F ratios were found, a Tukey's post hoc test was performed. All data are expressed as means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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Table 1 presents hemodynamic values at the
three workloads before and after intra-arterial infusion of
rauwolscine. There were significant increases in heart rate
(P < 0.001) and blood flow
(P < 0.001) as exercise intensity
increased. With the exception of blood flow and conductance in the
experimental limb, all of these variables remained unchanged following
the intra-arterial bolus of rauwolscine
(P > 0.05). Figure
1 is an original record from an individual
dog exercising on the treadmill at 3 miles/h. Intra-arterial infusion
of rauwolscine produced an immediate increase in blood flow in the
experimental limb, with no change in blood flow in the control limb. In
every dog, intra-arterial administration of rauwolscine abolished the
reduction in iliac blood flow produced by intra-arterial infusion of 10 µg of clonidine.
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Intra-arterial infusion of rauwolscine during exercise produced
substantial increases in blood flow at all exercise intensities (P < 0.001). However, the absence of
a significant drug times exercise intensity interaction
(P = 0.62) indicates that there were
no significant differences in the absolute changes in iliac blood flow
or conductance among the three different exercise intensities. In
contrast, there was a significant effect of exercise intensity on the
percent changes in iliac blood flow (P < 0.001) and conductance (P < 0.001) resulting from intra-arterial infusions of rauwolscine. The
percent increase in iliac conductance was greatest at 3 miles/h and
least at 6 miles/h, 10% grade (Fig. 2).
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Table 2 presents hemodynamic values at the
three workloads before and after intra-arterial infusion of prazosin.
There were significant increases in heart rate
(P < 0.001), blood pressure (P < 0.03), and iliac blood flow
(P < 0.001) with increases in exercise intensity. Furthermore, with the exception of blood flow and
conductance in the experimental limb, all these variables remained
unchanged following the intra-arterial bolus of prazosin (P > 0.05). Intra-arterial infusions
of prazosin during exercise produced marked increases in blood flow and
conductance at all exercise intensities
(P < 0.001). There was a
significant drug times exercise intensity interaction
(P < 0.01), such that there was an
inverse relationship between the absolute change in blood flow or
conductance and exercise intensity (P < 0.001). A similar relationship was revealed for the percent changes
in iliac blood flow and conductance after intra-arterial prazosin
infusion (P < 0.001). The increase
in iliac conductance was greatest at 3 miles/h and least at 6 miles/h,
10% grade (Fig. 2).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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Intra-arterial infusion of selective -adrenergic antagonists was
employed in conscious, exercising animals to acutely interrupt the
vasoconstrictor effects of exercise-induced sympathoexcitation. The
major new finding from these experiments is the demonstration of tonic
2-adrenergic receptor-mediated
vasoconstriction in working skeletal muscle during dynamic exercise,
even during intense exercise. Second, because the effects of
1- and
2-adrenergic receptor blockade
on vessel diameter are reflected by the percent change in conductance
(see below), we conclude that the magnitude of tonic -adrenergic
receptor-mediated vasoconstriction was inversely related to exercise
intensity. In other words, there was less sympathetic vasoconstriction
in active muscle as exercise intensity increased. However, the effect
of this tonic vasoconstriction on the restraint of blood flow was
different for 1- and
2-adrenergic receptors.
Exercise intensity did not appear to affect the magnitude of blood flow
restrained by 2-adrenergic
receptors, but there was an inverse relationship between tonic
1-adrenergic restraint of blood
flow and exercise intensity.
A number of previous studies (7, 12, 17, 19) did not demonstrate the
existence of sympathetic restraint of blood flow to exercising skeletal
muscle. Systemic administration of the nonselective -adrenergic
blocker phentolamine failed to alter blood flow to the working skeletal
muscle (12, 17, 19). In contrast, acute interruption of sympathetic
vasoconstriction (14, 29, 38) revealed that there was sympathetic
restraint of blood flow to exercising skeletal muscle. Two recent
studies (2, 28) that employed intra-arterial infusion of selective 1-adrenergic antagonists to
acutely interrupt sympathetic vasoconstriction provided clear evidence
of 1-receptor-mediated
vasoconstriction in working skeletal muscle. The findings of the
present study extend the previous results by demonstrating that there
is tonic 2-receptor-mediated
vasoconstriction in active skeletal muscle in the concious dog.
2-Adrenergic receptors are
found prejunctionally in proximity to the synapse as well as
postjunctionally on vascular smooth muscle. The prejunctional
2-receptor is thought to act in
an autoregulatory manner. Stimulation of prejunctional
2-receptors by norepinephrine
released into the synapse inhibits further release of norepinephrine.
To our knowledge there is no pharmacological agent that selectively
binds only prejunctional or postjunctional 2-adrenergic receptors. In the
present study, rauwolscine infusion caused an immediate vasodilation.
We interpret this vasodilation to mean that the main effect of the drug
was to antagonize postjunctional 2-receptors mediating
constriction. If the main effect had been on the prejunctional
2-adrenergic receptors, there
would have been greater release of norepinephrine from the synapse and
a vasoconstrictor effect. It must be recognized that prejunctional 2-receptors were probably also
antagonized by the rauwolscine. This could have increased
norepinephrine release and
1-receptor vasoconstriction
such that the magnitude of
2-receptor-mediated vasoconstriction was underestimated.
Postsynaptic 2-adrenergic
receptors contribute to vascular tone in canine skeletal muscles (11,
16). In rats, Faber (9) demonstrated that both
1- and
2-adrenergic receptors are
present on large arterioles, but only
2-receptors exist on the
terminal arterioles.
1-Adrenergic receptors appear
to exert the predominant control over the diameter of the large
arterioles, whereas 2-receptors control the diameter of the terminal arterioles (26). The present study
is the first to show tonic
2-adrenergic receptor-mediated vasoconstriction in active skeletal muscle during voluntary dynamic exercise. The design of these experiments in conscious animals precluded determination of the relative effects of adrenergic blockade
on larger arterioles versus terminal arterioles. However, it is likely
that intra-arterial infusion of -adrenergic antagonists in the
present study interrupted ongoing -adrenergic receptor-mediated vasoconstriction in the conduit arteries as well as the microcirculation.
Appropriate expression of data is essential for accurate interpretation in experiments designed to examine vasomotor function. Although not consistently used, it is recognized that vascular conductance, because of its linear relationship with flow, is a more appropriate expression of vasomotor function than of vascular resistance (18, 27). It has also been noted (33) that, when expressing changes in vascular tone from baseline, the percent change is more appropriate than the absolute change. Indeed, the percent change in conductance consistently reflects a calculable percent change in the radius of the vessel. If the desire is to compare the degree of vasoconstriction or vasodilation in a vascular bed, which by definition indicates a change in the vessel radius, the percent change in conductance more accurately reflects this change. These considerations are particularly important with comparisons of vasomotor tone between different exercise intensities where baseline blood flows are substantially different. Absolute changes in conductance would vary considerably when identical changes in vessel radius are imposed on differing baseline blood flows, whereas a given percent reduction in conductance reflects predictable percent reduction in the radius of the vessel despite differing baseline blood flows.
In the present study, whether expressed as a percent change or an
absolute change, there was an inverse relationship between the change
in iliac conductance with intra-arterial prazosin and exercise
intensity. However, examining the absolute change in conductance with
intra-arterial rauwolscine would lead one to conclude inappropriately
that there is the same degree of tonic vasoconstriction at each
workload. Although O'Leary et al. (28) reported a linear relationship
between 1-mediated
vasoconstriction (absolute change in conductance) and exercise
intensity, when these data are replotted as a percent change in
conductance, an inverse relationship between vasoconstriction and
exercise intensity is revealed. By examining the percent change in
iliac conductance in the present study, we conclude that intra-arterial
infusion of -adrenergic antagonists into the vasculature of skeletal
muscle produced less inhibition of vasoconstriction as exercise
intensity increased.
Direct recordings from sympathetic nerves have shown that increases in
exercise intensity produce increases in sympathetic outflow to visceral
organs (25) and skeletal muscle (6). We have previously reported (2),
that despite this increase in sympathetic outflow, there is an inverse
relationship between the magnitude of
1-adrenergic receptor-mediated
vasoconstriction in active skeletal muscle and exercise intensity.
However, in that study a fixed dose (100 µg) of prazosin was used and
may have been diluted by the higher blood flows at the higher exercise intensities. That limitation was overcome in the present study by the
dose adjustment of the -adrenergic receptor antagonists in
proportion to the exercise-induced increases in blood flow. Greater
doses of prazosin were administered at higher exercise intensities but
did not alter the inverse relationship between 1-adrenergic receptor-mediated
vasoconstriction and exercise intensity. A similar relationship was
seen between 2-adrenergic receptor-mediated vasoconstriction and exercise intensity. Thus we
conclude that the magnitude of tonic -adrenergic receptor-mediated vasoconstriction is inversely related to exercise intensity.
A decreased sensitivity to sympathetic stimulation or adrenergic
agonists in the skeletal muscle vasculature during exercise was first
described by Rein (30) and termed "functional sympatholysis" by
Remensnyder et al. (31). Although the existence of sympatholysis has
been controversial, it is clear that there is not total abrogation of
sympathetic control in active skeletal muscle (2, 28). Muscle perfusion is ultimately a competition between metabolic vasodilation and sympathetic vasoconstriction. The results from the
present study agree with other studies that show sympathetic vasoconstriction can be attenuated in active skeletal muscle by heavy
exercise (2, 15, 35). One proposed mechanism for sympatholysis involves
metabolic inhibition of
2-receptors. There appears to
be a differential sensitivity of
1- and
2-adrenergic receptors to
metabolic inhibition.
2-Adrenergic receptor-mediated vasoconstriction in skeletal muscle appears to be particularly sensitive to modest reductions in pH (20, 22, 36). In addition, hypoxia
(20, 36), ischemia (21), and muscle contractions (1, 37) have
been shown to inhibit
2-adrenergic receptor-mediated vasoconstriction in the arterial vasculature of skeletal muscle. On the
other hand, 1-adrenergic
receptor-mediated vasoconstriction appears to be unaffected by changes
in pH (20, 22, 36), hypoxia (20, 36), or ischemia (21). The
effect of electrically stimulated muscle contractions on
1-adrenergic receptor-mediated vasoconstriction is less consistent (1, 37). Anderson and Faber (1)
showed an attenuation of
1-adrenergic receptor-mediated vasoconstriction during intense muscle contractions, but Thomas et al.
(37) reported no attenuation of
1-adrenergic receptor-mediated vasoconstriction during muscle contractions. The present results showing inverse relationships between
1- and
2-adrenergic receptor-mediated vasoconstriction and exercise intensity are consistent with the concept
of exercise-induced sympatholysis. However, the demonstration of an
inverse relationship between vasoconstriction and exercise intensity
for both 1- and
2-adrenergic receptors does not
reflect a differential sensitivity of these two subtypes of receptors.
Although this discussion has focused on the relative degree of
vasoconstriction or vasodilation in the skeletal muscle vasculature, it
is recognized that the absolute changes in blood flow have physiological relevance in regard to blood pressure regulation. As
exercise intensity increases, sympathetic vasoconstriction in active
skeletal muscle becomes progressively more important for the regulation
of systemic blood pressure (32). The relationship between exercise
intensity and absolute changes in blood flow differed between prazosin
and rauwolscine, with
1-restraint of blood flow
decreasing across workloads and
2-restraint of blood flow
constant across workloads. One might assume that similar absolute
changes in blood flow with rauwolscine infusion indicate similar
contributions to systemic blood pressure regulation at each exercise
intensity. However, the effect of a given change in blood flow on blood
pressure regulation becomes smaller as total vascular conductance rises
with increasing exercise intensity. In other words, the change in mean
arterial pressure is inversely proportional to the total vascular
conductance. Because cardiac output and total vascular conductance
presumably increased across workloads in the present study, both
1- and
2-restraint of blood flow would
have less impact on blood pressure regulation at higher intensities.
In conclusion, the results from this study show that there is
considerable 1- and
2-adrenergic receptor-mediated
vasoconstriction in active skeletal muscles even at heavy exercise
intensities. In addition, the magnitude of tonic -adrenergic
receptor-mediated vasoconstriction in exercising skeletal muscles is
inversely related to exercise intensity.
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ACKNOWLEDGEMENTS |
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The authors acknowledge the valuable technical assistance of Paul Kovac. In addition, we gratefully acknowledge the donation of prazosin from Pfizer.
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FOOTNOTES |
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This project was supported by the Medical Research Service of the Department of Veterans Affairs and the National Heart, Lung, and Blood Institute.
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.
Address for reprint requests and other correspondence: J. B. Buckwalter, Anesthesia Research 151, VA Medical Center, 5000 W. National Ave., Milwaukee, WI 53295 (E-mail: jbuckwal{at}mcw.edu).
Received 7 October 1998; accepted in final form 9 March 1999.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS AND PROCEDURES
RESULTS
DISCUSSION
REFERENCES
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