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1 Medical Service, Nitric oxide (NO) is released into nasal
air, but its function is unknown. We hypothesized that nasal vascular
tone and/or flow influences temperature conditioning of nasal air and
that NO participates in this process. We measured nasal air temperature (via a thermocouple) and exhaled nasal NO release (by
chemiluminescence) in five humans and examined the effects of an
aerosolized vasoconstrictor (oxymetazoline), a vasodilator
(papaverine),
NG-nitro-L-arginine
methyl ester, an inhibitor of NO synthase, or saline
(control). Compared with saline (which caused no changes in nasal air temperature or exhaled NO release), oxymetazoline (0.05%)
reduced nasal air temperature and NO release (130.8 ± 15.1 to 81.3 ± 12.8 nl · min
temperature regulation; nose; vasoconstrictor; vasodilator
ENDOGENOUSLY PRODUCED NITRIC OXIDE (NO) is present in
the exhaled air of humans (14). The majority of exhaled NO
originates from the nasal passages (1, 13), but the function of NO in nasal physiology is poorly understood. One of the most important functions of the nasal passages is to condition the temperature of
nasal air (5). Inhaled air is efficiently warmed to temperatures within
a few degrees centigrade of core body temperature. During exhalation,
nasal air is cooled as heat is reabsorbed by the nasal mucosa, thereby
decreasing body heat loss to the environment. The mucosa of the nasal
passages is a highly vascularized tissue with subepithelial capillaries
and deeper venous sinusoids with smooth muscle in their walls (25),
which function as a type of capacitance system. Changes in nasal blood
flow and possibly venous capacitance have been postulated to be
involved in temperature conditioning of nasal air (5), but there is
little direct evidence linking changes in vascular tone or flow to
temperature changes in nasal air. The vasodilator functions of NO (21),
the presence of a well-developed venous capacitance system in the nose
(4), and the known modulation of microvascular flow and capacitance vessels by NO in other vascular beds (3) suggest a potential role for
NO in control of vascular tone in the nose and possibly a role in
temperature conditioning of nasal air.
We hypothesized that the tone of the nasal vasculature influences
temperature conditioning of nasal air and furthermore that NO has a
role in facilitating this function. To obtain evidence for these
hypotheses, we measured the temperature of nasal air in adult human
subjects and examined the effects of vasoactive agents on nasal air
temperature and NO release into nasal air. We found that vasoactive
agents directly affect temperature of nasal air as well as NO release
and that inhibition of NO release is associated with cooling of nasal
air. These findings are consistent with the concept that changes in
nasal vascular tone and/or flow modulate temperature conditioning of
nasal air and that NO participates in that function.
Studies were approved by the institutional Human Research Committee and
performed after written consent on human subjects (6 men and 2 women),
ages 21-53 yr. An investigational new drug permit was
obtained from the US Food and Drug Administration for use of
NG-nitro-L-arginine
methyl ester (L-NAME) in these experiments.
Measurement of nasal air temperature.
We used a wire thermocouple (type PT-6, Physitemp, Clifton, NJ) to
measure temperature of nasal air. The thermocouple was inserted into a
flexible feeding tube (Dobhoff), which was scored by centimeters, with
the tip of the thermocouple as the reference (zero) point. The tip of
the thermocouple was positioned at a distal, recessed opening in the
flexible tube so that the thermocouple could be exposed to nasal air
without contacting the nasal mucosa directly. The response time
(0-90% full scale) of the thermocouple was 410 ± 20 ms
(n = 5 measurements) in the
temperature range of our experiments. We calibrated the thermocouple
against a mercury thermometer by placing both thermocouple and
thermometer in water at three different temperatures over the range
relevant to our experiments. The tube was then placed into one nare of
the subjects, and the temperature of nasal air was measured at each
centimeter to a depth of 9-10 cm from the nasal sill while the
seated subjects breathed through the nose with the mouth closed. At
each centimeter position, the thermocouple tip was held in place for
five to six tidal breaths or until the temperature was stable. The
average inspiratory and expiratory temperature over three breaths was recorded. The temperature signal was processed by a direct-channel amplifier (Omega Engineering, Stamford, CT) and recorded directly on a
strip-chart recorder (Gould Brush, Cleveland, OH).
Measurements of exhaled nasal NO release.
For measurements of NO release, subjects breathed with tidal breaths
through the nose with mouth closed for 2 min into a face mask. The face
mask was attached to a two-way valve to allow inhalation of air from a
reservoir bag (filled with NO-free air from a compressed air tank) and
collection of the exhaled air in a Mylar balloon. This bag
was previously shown to be impermeable to and nonreactive with NO (16).
After the 2-min collection, the concentration of NO in the bag was
measured in a chemiluminescence analyzer (model 270B, Sievers
Instruments), and then the volume of the bag was measured in a Tissot
gasometer. The analyzer responded in a linear fashion over the range of
NO concentrations of interest (from 2 to 200 parts/billion) with a
0-90% full-scale response time of 6.5 s. We calibrated the
analyzer with dilutions of a known NO source (40 parts/million in
nitrogen) by precise dilutions of the calibration gas in compressed air
(NO free) by using a calibrated 2-liter syringe. NO release (nl/min)
into nasal air was calculated as the product of NO concentration in the
collection bag (parts/billion, or nl/l) and the minute ventilation
through the nose (l/min). Results are expressed as nanoliters per
minute per square meters of body surface area.
Experimental protocols.
In the first set of experiments, we characterized the nasal air
temperature changes during nasal breathing and then measured the effect
of aerosolization of normal saline (3 ml) to the nasal mucosa on
exhaled nasal NO release and temperatures of nasal air to a depth of
9-10 cm into the nasal passages. Normal saline was studied as a
control for the effects of aerosolization of room temperature liquid
into the nasal passages on temperature conditioning of nasal air and NO
release and because saline served as the vehicle for other vasoactive
agents in subsequent experiments. Five subjects were studied in the
sitting position. In the next series of experiments, we measured the
effect of aerosolization of oxymetazoline hydrochloride (0.05% without
benzalkonium), a known nasal vasoconstrictor, or papaverine
hydrochloride (0.01 M), a vasodilator, respectively on exhaled NO and
nasal air temperature in five subjects. Next, we determined the
dose-response effect of aerosolization of a solution of
L-NAME to the nasal mucosa on
exhaled NO during nasal breathing in three subjects. Finally, we
measured the effect of a near-maximal effect dosage of
L-NAME (0.5 M) on exhaled NO and nasal air temperature in five subjects. Control experiments for this
last experiment included testing of a hypertonic (5%) saline solution
(1,710 mosM) because the L-NAME
solution used was hypertonic (1,498 mosM) relative to normal saline
(310 mosM).
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
1 · m2;
P < 0.01). Papaverine (0.01 M)
increased nasal air temperature and NO release (131.8 ± 13.1 to
157.2 ± 17.4 nl · min1 · m2;
P < 0.03).
NG-nitro-L-arginine
methyl ester reduced nasal air temperature and NO release (123.7 ± 14.2 to 44.2 ± 23.7 nl · min1 · m2;
P < 0.01). The results suggest that
vascular tone and/or flow modulates temperature conditioning and that
NO may participate in that function.
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
Data analysis. All data are reported as means ± SE. Differences in temperature or nasal NO release were compared by using paired Student's t-tests. A P value of <0.05 was considered significant.
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METHODS
RESULTS
DISCUSSION
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Measurements of nasal air temperature and nasal NO release under
control conditions.
The pattern of temperature conditioning of nasal air during inhalation
and exhalation in five adult subjects is shown in Fig. 1. During inhalation, the temperature of
nasal air increased with distance into the nasal passages. The greatest
change in temperature occurred in the first 4 cm, and the temperature
reached a plateau thereafter (Fig. 1). During exhalation, mean nasal
air temperatures were slightly greater, and the air temperature
decreased progressively as nasal air approached the external nares.
Nebulization of normal saline (3 ml) into the nasal passages had no
effect on temperature conditioning of nasal air when it was measured
hourly over a 3-h period after administration of saline (data not
shown).
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1 · m2
in five subjects in the sitting position, similar to measurements made
previously in our laboratory (16). Nasal NO release was unaffected by
nebulization of normal saline (3 ml) into the nasal passages. The
values for mean NO release at 1, 2, and 3 h after nebulization of
normal saline were 115.5 ± 22.3, 124.5 ± 10.8, and
128.2 ± 18.5 nl · min1 · m2,
respectively (P = not significant vs.
baseline for each hour) in the five subjects.
Effects of oxymetazoline on temperature conditioning of nasal air
and nasal NO release.
The 
-adrenergic agonist oxymetazoline hydrochloride (0.05%) reduced
the temperature of nasal air progressively over a 3-h period after
topical administration of the drug (Fig. 2,
A and B). For clarity of presentation,
only the 3-h data (which was the maximal effect) are shown in Fig. 2
and subsequent figures. Both the slope of temperature change with
distance into the nose and the plateau levels of temperature were
reduced after oxymetazoline. Nasal NO release was also reduced to
~60% of the baseline (control) value after 3 h (from 130.8 ± 15.1 to 81.3 ± 12.8 nl · min1 · m2;
P < 0.01; Fig.
2C). No changes in pulse rate or
blood pressure were found after aerosolization of oxymetazoline into
the nasal passages.
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Effects of papaverine on temperature conditioning of nasal air and
nasal NO release.
The vasodilator papaverine hydrochloride (0.01 M) increased the
temperature of nasal air 2-3 cm into the nose during inhalation and at 3 cm from the opening of the nares during exhalation in five
subjects (Fig. 3,
A and
B). The mean value of NO release into the nasal passages was also increased 3 h after papaverine (from
131.8 ± 13.1 to 157.2 ± 17.4 nl · min1 · m2;
P < 0.03; Fig.
3C). No significant changes in pulse
rate or blood pressure were found after topical aerosolization of
papaverine into the nasal passages.
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Dose-response effects of L-NAME on
nasal NO release.
In three subjects, we determined the dose-response relationship of
L-NAME on nasal NO release (Fig.
4). In Fig. 4, nasal NO release is shown on
the y-axis, and the solutions tested
are indicated on the x-axis. Compared
with the effects of normal saline, topical administration of
L-NAME (
0.1 M) decreased
release of NO into nasal air 3 h after the topical administration of
the drug to the nasal mucosa. The
L-NAME solutions used were
hypertonic relative to normal saline (measured osmolarity of a 1 M
solution of L-NAME = 1,498 mosM). However, hypertonicity did not account for the L-NAME effect because a
hypertonic (5%) solution of saline (1,710 mosM) did not alter NO
release from the nose (Fig. 4). No significant changes in pulse rate or
blood pressure were found after topical aerosolization of
L-NAME into the nasal passages.
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Effects of L-NAME on temperature
conditioning of nasal air and nasal NO release.
Topical application of an aerosol of
L-NAME (0.5 M, 3 ml) to the
nasal mucosa decreased the temperature of nasal air 4-9 cm into
the nose during inhalation and exhalation in five subjects (Fig.
5, A and
B). Compared with baseline
measurements, nasal air temperature did not reach a plateau during
either inhalation or exhalation. The mean value for nasal NO release
was reduced to ~35% of the baseline (control) value 3 h after
L-NAME (from 123.7 ± 14.2 to 44.2 ± 23.7 nl · min1 · m2;
P < 0.01; Fig.
5C).
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METHODS
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DISCUSSION
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A major function of the nasal passages is the temperature regulation of
inhaled and exhaled air. The findings of our study were that topically
applied vasoactive agents modify both the temperature conditioning of
inhaled and exhaled air and the release of NO into nasal passages.
Oxymetazoline, an -adrenergic agonist causing vasoconstriction,
reduced the heat exchange between mucosa and nasal air and was
associated with a decrease in NO release. Papaverine, a vasodilator,
increased the heat exchange between mucosa and nasal air and was
associated with increased release of NO. Finally, an inhibitor of NO
synthase (L-NAME) reduced the heat exchange between mucosa and nasal air and also reduced the release
of NO. These findings are consistent with the concept that changes in
nasal vascular tone and/or flow modulate temperature conditioning of
nasal air and that NO participates in that function.
The nasal mucosa has an extensive vasculature that is presumed to function in temperature conditioning of nasal air (25). At least five different types of vessels can be identified in the nasal microvasculature, including arterioles, sinusoids, capillaries, venules, and arteriovenous anastomoses, although the existence of the latter is controversial. The control and function of these various structures are poorly understood (25). Cole (5) has pointed out not only that the nasal passages function as an efficient heat exchanger but also that the ability of the nose to heat and humidify inhaled air can be easily overcome under adverse environmental conditions. The majority of heat added to inspired air in the nose comes from heat recovered by the nasal mucosa from the exhaled air of the previous breath. The balance of heat required to warm inspired air presumably is provided by blood flow to the nasal mucosa, although there is little direct experimental evidence for this premise, probably because of the difficulty in accurate measurement of total nasal blood flow. Cole (4) found that administration of the vasoconstrictors ephedrine (1%) or amphetamine was associated with a decrease in the nasal temperatures of inspired air. Drettner and co-workers (8) found that topical administration of oxymetazoline decreased the air conditioning capacity of the nose. Local microcirculatory measurements with laser-Doppler velocimetry have confirmed that oxymetazoline reduces blood flow to the nasal mucosa within the measurement area of the probe (9). There is less information on the effects of vasodilation on temperature conditioning of nasal air. Systemic injection of priscol, a drug associated with increased blood flow, caused an increase in the inspired air temperature (4). Vasodilators such as salbutamol and histamine cause an increase in nasal airflow resistance (24), which indirectly assesses the volume of blood in the nasal mucosa. However, the effects of vasodilation or increased blood flow on temperature conditioning of nasal air have not been well studied. Of interest, exercise with its attendant increase in total blood flow is associated with decreased airflow resistance in the nasal cavities, suggesting a decrease in blood volume of the nasal mucosa (11). However, passive hyperthermia of humans by immersion to the neck in a heated water bath increases nasal blood flow (23), leading to the suggestion that the nasal passages may help eliminate body heat to cool the brain during hyperthermia.
Our method of measurement of nasal air temperatures used a thermocouple threaded through a Dobhoff catheter, which protected the tip of the thermocouple against contact with the nasal mucosa. For most of the length of nasal cavity in which measurements were made, the temperature tracing showed variation between inspiration and expiration, confirming that the catheter tip was positioned in the nasal airstream. However, in some subjects, inspiratory and expiratory temperatures were not different when the catheter reached distances between 8 and 10 cm into the nasal cavity. When withdrawn, the catheter was often moist with nasal secretions in these subjects, so it is possible that the secretions formed a bridge between the mucosa and the thermocouple in these cases, rendering distinctions between inspiratory and expiratory temperatures impossible. An additional methodological concern is that nasal airflow might have changed with administration of vasoactive agents, with secondary effects on nasal NO release. However, administration of oxymetazoline, papaverine, or L-NAME caused no significant changes in resting minute ventilation, respiratory rate, or time of inspiration or expiration (data not shown), suggesting that airflow rate was not affected by these agents. Another methodological issue concerned our measurements of exhaled NO release. Presently, there is no standardized method of measuring total release of NO into nasal air. In previous studies (16), we used the methods outlined in this study while characterizing the contribution of the nasal passages to release of NO into the exhaled air. It should be noted, however, that measurement of only exhaled air underestimates the total release of NO by the nasal passages because NO released during inhalation is carried into the lower airway where it is taken up. In our prior study, we estimated that 30-40% of NO inhaled was taken up by the lower airways (16). Gerlach et al. (13) estimated that 50-70% of nasal NO is taken up in the lower airways. Differences in these estimates may be related to different methodologies in these two studies.
The presence of NO in exhaled air of humans, and the subsequent finding that the majority of exhaled NO is released into the nasal passages, raises the question of how NO functions in nasal physiology. NO is involved in myriad physiological functions, including vasodilation (21), bacteriostatic and fungistatic functions (21), cell-mediated immunity against neoplasms (21), and neurotransmission (2). Each of these functions has relevance to the nasal cavity, but none has been linked directly to the high levels of NO found in the nasal passages. The physical characteristics of NO, lipophilic and possessing a high partition coefficient at an air-liquid interface, favor its release into air in both the lungs and nasal passages. For these reasons, it seems likely that NO released into nasal air directly reflects tissue levels, although this relationship has not been directly established. Both constitutive (type III) and inducible (type II) forms of NO synthase (NOS), the enzyme that generates NO during the conversion of L-arginine to L-citrulline, have been identified by immunohistochemistry in the nasal mucosa (12). Further studies in which in situ hybridization was used found that type III NOS mRNA is present in endothelium, surface epithelium, and glands, whereas type II NOS is largely found in inflammatory cells (12). A calcium-independent type of type II NOS has also been identified in the epithelium of the paranasal sinuses (19). A considerable portion of exhaled NO from the lower airways may be derived from type I NOS (6), but this has not been investigated in the nasal passages, although type I NOS is present on nerves of the nasal mucosa (22). To date, the function of NO in nasal physiology has not been elucidated. Lundberg and co-workers (17) found high concentrations of NO in the paranasal sinuses and have hypothesized that NO functions to control bacterial growth in the sinuses. NO may also be involved in the modulation of ciliary beat frequency in airway epithelium (15) and is deficient in patients with Kartagener's syndrome (18). However, the exact role of NO in nasal physiology remains poorly understood.
Our findings suggest a potential role for NO in modulation of the vascular changes necessary for temperature conditioning of nasal air and, possibly by extension, thermoregulation in humans. Of interest, there is evidence that NO plays a role in the regulation of heat loss through the skin in exercising horses via stimulation of the sweating rate (20). In contrast, NO is apparently not responsible for cutaneous vasodilation during body heating in humans (7). In our study, inhibition of NOS with L-NAME decreased NO release into nasal air and reduced the temperature of both inhaled and exhaled air. The vasoconstrictor oxymetazoline has previously been shown to decrease release of NO into nasal air (10). Oxymetazoline was associated with similar effects to those of L-NAME, whereas the vasodilator papaverine caused the opposite effects of increased NO release and increased temperature of nasal air. These data suggest that NO release is inversely related to vascular tone in the nasal mucosa. The mechanisms for local NO release in the vasculature are not entirely clear, but pulsatile flow and shear stress are probably both involved (21). Hence, a reduction in flow induced by oxymetazoline and an increase in flow after papaverine might be expected to cause a decrease and increase in NO release, respectively. Neither oxymetazoline nor papaverine has been directly linked to release of NO to our knowledge. However, our experiments do not define whether NO is responsible for changes in vascular tone associated with the application of oxymetazoline or papaverine or whether it is released in response to changes in vascular tone produced by these agents.
In summary, we found that vasoactive agents directly affect temperature of nasal air as well as NO release and that inhibition of NO release is associated with cooling of nasal air. These findings are consistent with the concept that changes in nasal vascular tone and/or flow modulate temperature conditioning of nasal air and that NO participates in that function.
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ACKNOWLEDGEMENTS |
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This work was supported by a grant from the Murdock Foundation.
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FOOTNOTES |
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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: W. E. Holden, Pulmonary and Critical Care Sect., Portland Veterans Affairs Medical Center, 3710 SW US Veterans Rd., Portland, OR 97201 (E-mail: holden.williame{at}portland.va.gov).
Received 9 July 1998; accepted in final form 27 May 1999.
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RESULTS
DISCUSSION
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;
A) increased during inhalation and
reached a plateau at 4 cm into the nasal cavity. Mean air temperatures
during exhalation (
; B) were
slightly greater than inhaled air temperatures and decreased as the
opening of the nares was approached.
, 
, and
open bar). Oxymetazoline reduced nasal air temperatures during both
inhalation and exhalation and reduced release of nasal nitric oxide.
* P < 0.05 vs. control
(baseline) measurements.
