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Equine Centre, The Animal Health Trust, Newmarket, Suffolk CB8 7DW, United Kingdom
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
ABSTRACT 
Mills, Paul C., David J. Marlin, Caroline M. Scott, and
Nicola C. Smith. Nitric oxide and thermoregulation during exercise in the horse. J. Appl. Physiol. 82(4):
1035-1039, 1997.
The effect of inhibition of nitric oxide
production on sweating rate (SR) and on core, rectal, and tail skin
temperatures was measured in five Thoroughbred horses during exercise
of variable intensity on a high-speed treadmill. A standard exercise
test consisting of three canters [~55% maximum
O2 uptake
(
O2 max)], with
walking (~9%
O2 max) and trotting
(~22% O2 max)
between each canter, was performed twice (control or test), in random
order, by each horse.
NG-nitro-L-arginine methyl ester
(L-NAME; 20 mg/kg), a
competitive inhibitor of nitric oxide synthase, was infused into the
central circulation and induced a significant reduction in the SR
measured on the neck (31.6 ± 6.4 vs. 9.7 ± 4.2 g · min
1 · m2;
69%) and rump (14.7 ± 5.2 vs. 4.8 ± 1.6 g · min1 · m2;
67%) of the horses during canter (P < 0.05). Significant increases in core, rectal, and tail
skin temperatures were also measured (P < 0.05).
L-Arginine (200 mg/kg iv)
partially reversed the inhibitory effects of
L-NAME on SR, but core, rectal,
and tail skin temperatures continued to increase
(P < 0.05), suggesting a cumulation
of body heat. The results support the contention that nitric oxide
synthase inhibition diminishes SR, resulting in elevated core and
peripheral temperatures leading to deranged thermoregulation during
exercise. The inhibition of sweating by
L-NAME may be related to
peripheral vasoconstriction but may also involve the neurogenic control
of sweating.
sweating rate; NG-nitro-L-arginine methyl ester; nitric oxide
INTRODUCTION EVAPORATIVE HEAT LOSS is essential for heat dissipation
during hyperthermia (3). Species differences are found in the relative contribution of respiratory heat exchange and skin evaporation, and
skin sweating is the primary mechanism of evaporative heat loss in
horses and humans (3, 10, 37). The capacity of the skin to
receive a high blood flow is second only to muscle (23), and it is,
therefore, not surprising that thermoregulation is a major function of
the cutaneous circulation (35).
Exercise induces a rise in body temperature, and a significant
correlation exists between sweating rate (SR) and body temperature (18). Strenuous exercise will also enhance blood flow to the skin (26).
The control of both skin blood flow and sweating appears to be mediated
by the sympathetic nervous system (2, 15, 23), although the extent of
humoral regulation and the particular receptor types responsible for
sweat secretion vary among species (2, 23). The majority of mammalian
eccrine sweat glands are stimulated predominantly by cholinergic
receptors while also being responsive to adrenergic stimulation (27), but equine apocrine sweat glands are under mainly
The role of nitric oxide (NO) in the control of sweating is unknown.
The onset of sweating correlates with cutaneous blood flow (23), and NO
regulates regional blood flow by relaxing vascular smooth muscle,
inducing vasodilation, and opposing pressor responses (6,
17). NO has been shown to dilate cutaneous vasculature (4,
7) while inhibitors of NO synthase (NOS; the enzyme responsible for NO
production), such as
NG-nitro-L-arginine methyl ester
(L-NAME), have been shown to
cross the blood-brain barrier (25) and exert a pressor response (6, 12), probably by enhancing central sympathetic activity (24, 34). The
importance of NO in cutaneous vasodilation during body warming is
uncertain (4, 32) while the contribution of NO to exercise-induced
vasodilation remains controversial (5, 8, 9, 12). Moreover,
investigation of skin blood flow during exercise in humans has
suggested a separate neuronal control of sudomotor and active
vasodilatory function in the skin (11, 13).
Endothelial cell NOS (ecNOS) normally regulates basal vascular tone
while a neural constitutive isoform (ncNOS) is involved in central and
peripheral neurotransmission, including the nonadrenergic noncholinergic nervous system (17). Taylor and Bishop (32) have shown that NO was inherent in the neurogenic control of
thermoregulatory vasodilation in response to body warming. In addition,
Nagashima et al. (20) reported that
L-NAME inhibited the
norepinephrine-induced increase in blood flow through brown adipose
tissue, a major thermogenic organ. ncNOS has been isolated
in sympathetic preganglionic neurons and in spinal cord neurons, which
mediate sympathetic output to various peripheral organs (36), and,
because the sympathetic nervous system is the principal regulator of
sweating (23), NO may modulate the sweating response by affecting the
sympathetic sudomotor activity.
In this study, we investigated the effects of inhibition of NO
production on SR and on core, rectal, and tail skin temperatures in the
horse during exercise.
L-Arginine, a substrate for NOS, was also given to competitively reverse the effects of
L-NAME and to measure any
potentiation of NOS by its substrate.
METHODS
2-adenergic control (1, 37).
O2 max),
was ~9% for 1.7 m/s, 22% for 3.7 m/s, and 55% for 8 m/s (personal
communication). The horses completed the SET twice, 2 days apart, as a
control or test SET in random order. In the test run,
L-NAME (20 mg/kg; Sigma
Chemical, Poole, UK) was infused into the pulmonary artery (described
in Measurement of core, rectal, and tail skin
temperatures) over 5 min immediately after the first
canter, and L-arginine (200 mg/kg; Sigma Chemical) was injected by rapid intravenous injection immediately after the second canter for both control and test SETs. The dose rates of
L-NAME and
L-arginine were based on a similar study during exercise in sheep (12, 14). The dose of
L-NAME, in particular, was based
on its inhibitory effects on cerebral and myocardial blood flow during
hypoxia in the conscious dog (1) and the increase in pulmonary vascular
resistance and tone during exercise in the sheep (12, 14), effects that
may be modulated by NO.
The environment conditions within the treadmill room were maintained at
25°C and 55% relative humidity (RH) by an air-conditioning system
(Deltaclima VAH50, Rapid Airconditioner, Haverhill, UK) with a
supplementary humidifier (Electrovap Super ELS, Devatec, UK) and
a custom-made additional cooling/heating bank (Adcocks Refrigeration,
Cambridge, UK). The output of the air-conditioning unit
was ducted to the front of the horse, and the temperature and RH of the
air leaving the duct were monitored and recorded with HMP35B
temperature/RH sensors (Vaisala; Helsinki, Finland). Immediately in front of the air-conditioning outlet duct was a large
fan (66-cm diameter, Solar and Palau). This delivered the conditioned
air over the horse at a speed equivalent to the treadmill belt speed.
Measurement of core, rectal, and tail skin temperatures.
A catheter introducer (8-Fr, Arrow, Reading, PA) was placed into the
left jugular vein by using local anesthesia (2% Xylocaine, Astra
Pharmaceutical) before the commencement of exercise. A Swann-Ganz thermodilution catheter (7-Fr Criticath, Spectramed) was advanced into
the pulmonary artery to measure core (central body) temperature. Correct placement was verified by following pressure traces obtained with a strain-gauge sensor (T-150-AD, Viggo-Spectramed, Swindon, UK).
L-NAME was infused (4.0 mg · min1 · kg1)
via the distal port of the thermodilution catheter, and
L-arginine was given via the
side arm of the introducer.
Rectal temperature was obtained by using a probe containing a
temperature sensor integrated circuit (LM35CZ) inserted into the rectum
to a depth of 25 cm. Tail skin temperature, a sensitive indicator of
the blood temperature within the ventral coccygeal artery (unpublished
results), was measured on the underside of the tail with a YSI 4400 series thermistor probe (Yellow Springs Instruments) and a temperature
amplifier (model 13-4615-47, Gould Electronics). The thermistor bead
was maintained in place directly over the ventral coccygeal artery with
a skin adhesive (Vetbond, 3M, Bracknell, UK) and secured by a synthetic
bandage (Vetrap, 3M). All temperature sensors were calibrated before
and after use in water baths set at ~37 and 42°C, respectively,
by using a precision mercury thermometer with a resolution of
0.05°C.
Measurement of SR.
SR was measured by using the method described by Scott et al. (28).
Briefly, lightweight plastic capsules were attached by using skin
adhesive (Vetbond) to the neck and the rump (over the middle gluteal
muscle). A stream of dry air was passed over the horses' skin within
the capsule, and the difference in temperature and RH was monitored by
HMP35B temperature/RH sensors. Output from the probes was used to
calculate the water content of the air (and thereby SR) via computer.
Measurements of temperatures and SR were recorded at the following
times during the experiment:
1) at rest,
2) after 9 min of walk;
3) after 4 min of trot,
4) after 4 min of canter,
5) after 5 min of walk (recovery),
6) after 24 min of walk,
7) after 4 min of trot,
8) after 4 min of canter,
9) after 5 min of walk (recovery),
10) after 14 min of walk,
11) after 4 min of trot, 12) after 4 min of canter, and
13) after 5 min of walk (recovery).
Statistical analysis.
Data are presented as means ± SD. Significant differences between
SRs and temperature measurements were calculated by using two-way
analysis of variance. Dunnett's
t-test was applied as a post hoc test.
Differences between control and test SETs were considered significant
at the 95% level (P < 0.05).
RESULTS
1 · m2)
and neck (31.6 ± 6.4 vs. 9.7 ± 4.2 g · min1
· m2)
measurements. L-Arginine
partially reversed the effects of
L-NAME, and the SRs measured at
both sites were slightly lower than when measured at comparative times
during the control SET.
Body temperatures. Administration of L-NAME induced a significant increase (P < 0.05) in core temperature (Fig. 2A) during the second canter (39.7 ± 0.2 vs. 40.6 ± 0.7°C). The core, rectal, and tail skin temperatures (Fig. 2, A-C) continued to rise after the second canter and were significantly higher (P < 0.05) than corresponding stages in the control SET despite the administration of L-arginine.
) and test (
) standard exercise tests.
NG-nitro-L-arginine methyl ester (20 mg/kg; solid arrow) was infused over 5 min (horizontal line) after
first canter in test standard exercise test only. * Significant
difference between control and test standard exercise tests,
P < 0.05.
DISCUSSION
Two sites were chosen to measure SR in the horse because the onset and rate of sweating can vary with different body sites (10, 19). The results from our study show that nonspecific inhibition of NOS activity substantially reduces the SR in the horse from both the neck and rump regions. Consequently, a rise in core temperature was detected during moderate exercise. This was expected because the skin is the primary site of evaporative heat loss in several mammals, including humans and horses (3, 10, 37). An incomplete return of sweating activity after L-arginine was given combined with a central cumulation of heat acted to significantly increase both tail skin and rectal temperatures during the third canter of the test SET.
The exact mechanism by which L-NAME restricted SR during exercise is uncertain. Exercise will both enhance blood flow to the skin and increase body temperature (24). Increases in skin blood flow (23, 27) and body (26) or blood temperature (31) have been shown to correlate with SR, leading to a postulated link between SR and active vasodilation (29). Taylor and Bishop (32) suggested that NO is the mediator of cutaneous thermoregulatory vasodilation and that, because inhibition of ecNOS activity will induce a vascular pressor response at rest and during exercise (12, 17), the reduction in the sweating response in the horse during exercise may, therefore, reflect restriction of skin blood flow after L-NAME is given. Indeed, our laboratory has recently demonstrated that L-NAME will induce a pressor response in the horse during moderate exercise without an effect on cardiac output (28). It is unfortunate that we were unable to measure cutaneous blood flow or skin temperature in the exercising horse and, therefore, cannot conclusively describe the relationship between sweating and the pressor effect of L-NAME. The rise in tail skin temperature after L-NAME is given is misleading and appears to indicate a peripheral vasodilation. However, tail skin temperature is a sensitive indicator of blood temperature within the underlying ventral coccygeal artery (28), and blood reaching the peripheral circulation was comparatively hotter after L-NAME was given. Furthermore, inhibitors of ecNOS predominantly affect the smaller resistance arterioles (17), whereas the relative contribution of NO to blood flow during exercise in this relatively major artery of the equine tail is uncertain.
Restricted cutaneous blood flow after inhibition of ecNOS is not,
however, a convincing explanation for the reduction in SR. It has
recently been demonstrated with the use of labeled microspheres that
moderate exercise (~60%
O2 max) induced a
relatively small increase in skin blood flow (D. R. Hodgson, F. McConaghy, and R. J. Rose, personal communication), despite the fact
that sweating is the predominant thermoregulatory mechanism in the
horse (10, 37). Furthermore, NO does not appear to play a
major role in cutaneous vasodilation during body heating (4) or
exercise-induced metabolic arterial vasodilation in the forearm (5) of
humans. Kane et al. (12) also suggested that while NO will dilate
vasculature at rest, this basal release will oppose 
-adrenergic
vasoconstriction during exercise without additional release of NO. The
link between active cutaneous vasodilation and sweating has also been
questioned. For example, the core temperature threshold for the
initiation of sweating in humans is unaffected by exertion, whereas a
higher core temperature is required for active cutaneous
vasodilation during exercise (11, 13). Similarly, Taylor et al.
(33) reported that the core temperature threshold for upregulation of
cutaneous blood flow increases with exercise intensity and suggested
that the pressor response at the onset of exercise successfully antagonizes active thermoregulatory vasodilation. Such findings led
Kellogg et al. (13) to suggest separate neural control of sudomotor and
active vasodilatory functions.
An alternative explanation of the relationship between SR and NO could be the modulation of neural activity, particularly because regional analgesia will impair the cutaneous sweating response to body warming (21). NO appears to play a key role in neurogenic cutaneous vasodilation in rabbits (32) and humans (4). More importantly, NOS has been isolated in sympathetic preganglionic neurons and in spinal cord neurons, which mediate sympathetic output to various peripheral organs (36). For example, nonspecific inhibition of NOS has been shown to inhibit the norepinephrine-induced increase in blood flow through brown adipose tissue, a major thermogenic organ (20). In addition, a central mechanism is thought to be responsible for the regulation of active vasodilation and sweating in response to a rise in body temperature (30), and L-NAME has been shown to cross the blood-brain barrier (25) and affect central sympathetic activity (7, 24, 34). An interesting clinical observation during our study was ataxia and mild depression in the horses after L-NAME is infused. They did not appear to be induced by hyperthermia because the neurological clinical signs were no longer apparent after L-arginine administration, despite further increases in body temperatures. L-NAME has similarly been reported to depress cerebral neural pathways in sheep (25). Because the sympathetic nervous system is the primary mechanism regulating both skin blood flow and sweating (2, 15, 23), altered peripheral and/or sympathetic activity after giving L-NAME may have disrupted sudomotor control in the horse.
Administration of L-arginine to the horses partially reversed the effects of L-NAME, which acts as a competitive inhibitor of NOS (17). Small discrepancies between SRs and temperatures in the test SET after L-arginine is given, compared with the control SET, may reflect insufficient time for L-arginine to completely reverse the effects of L-NAME. However, L-NAME has been reported to be a nonspecific inhibitor of NOS and, particularly at higher dose rates, may induce muscarinic effects on the vasculature (22). Furthermore, L-NAME has a greater isoform specificity for ncNOS than for ecNOS (22). Hirai and co-workers (9) reported that administration of L-arginine at a rate of 300 mg/kg did not return mean arterial pressure to pre-L-NAME levels, which, similar to our study, may reflect some effects of L-NAME other than specific inhibition of NOS. Of greater physiological relevance was the lack of potentiation of NOS activity by the supraphysiological dose rate of L-arginine given. Similar findings have been reported in humans and sheep (12, 17), which suggests that the activity of NOS is not normally substrate dependent.
In summary, nonspecific inhibition of NOS significantly reduced the SR and increased the body temperatures of the horse during exercise. This effect may be related to peripheral vasoconstriction but suggests a possible modulation by NO of central and/or peripheral sympathetic control of sweating.
ACKNOWLEDGEMENTS
This study was made possible by the generous support of the Marjorie Coote Animal Charity Trust Fund.
FOOTNOTES
Address for reprint requests: P. Mills, Equine Centre, The Animal Health Trust, PO Box 5, Newmarket, Suffolk CB8 7DW, UK.
Received 8 July 1996; accepted in final form 22 November 1996.
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R. C. H. Barros and L. G. S. Branco Effect of nitric oxide synthase inhibition on hypercapnia-induced hypothermia and hyperventilation J Appl Physiol, September 1, 1998; 85(3): 967 - 972. [Abstract] [Full Text] [PDF]
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M. Manohar and T. E. Goetz L-NAME does not affect exercise-induced pulmonary hypertension in Thoroughbred horses J Appl Physiol, June 1, 1998; 84(6): 1902 - 1908. [Abstract] [Full Text] [PDF]
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M. J. Joyner Invited Editorial on "Nitric oxide and thermoregulation during exercise in the horse" J Appl Physiol, April 1, 1997; 82(4): 1033 - 1034. [Full Text] [PDF]
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