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1 Faculdade de Odontologia de Ribeirão Preto, 2 Escola de Enfermagem de Ribeirão Preto, and 3 Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, 14040-904 Ribeirão Preto, São Paulo, Brazil
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ABSTRACT |
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 Top
 Abstract
 Introduction
Materials and methods
Results
Discussion
References
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The present study was designed to test the hypothesis that arginine vasopressin (AVP) mediates hypoxia-induced anapyrexia. The rectal temperature of awake, unrestrained rats was measured before and after hypoxic hypoxia, AVP-blocker injection, or a combination of the two. Control animals received saline injections of the same volume. Basal body temperature was 36.52 ± 0.29°C. We observed a significant (P < 0.05) reduction in body temperature of 1.45 ± 0.33°C after hypoxia (7% inspired O2), whereas systemic and central injections of AVP V1- and AVP V2-receptor blockers caused no change in body temperature. When intravenous injection of AVP blockers was combined with hypoxia, we observed a reduction in body temperature of 1.49 ± 0.41°C (V1-receptor blocker) and of 1.30 ± 0.13°C (V2-receptor blocker), similar to that obtained by application of hypoxia only. Similar results were observed when the blockers were injected intracerebroventricularly. The data indicate that endogenous AVP does not mediate hypoxia-induced anapyrexia in rats.
temperature; hypothermia
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INTRODUCTION |
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Top
Abstract
Introduction
Materials and methods
Results
Discussion
References
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IN ORGANISMS ranging from protozoans to mammals, body temperature (Tb) decreases in response to a lack of O2 (3, 34, 35). The importance of this response is emphasized by reports that show an increase in survival of the tested species if the subjects are allowed to become hypothermic during hypoxia exposure (12). Anapyrexia (a regulated decrease in Tb) can be a beneficial response in hypoxic animals, because it reduces O2 consumption according to the Q10 effect; produces a leftward shift of the oxyhemoglobin dissociation curve, with the resulting improvement of O2 loading in the lungs; and decreases ventilation, with the resulting blunting in the energetically costly responses to hypoxia (cf. Ref. 35). Although this protective response is extremely widespread among taxa, little is known about the mechanisms that mediate hypoxia-induced anapyrexia.
Several candidates have been suggested (see Ref. 35) as potential mediators of anapyrexia, among them arginine vasopressin (AVP). In support of this hypothesis are the findings that hypoxia causes an increase in the plasma levels of AVP in mammals (10, 24) and that AVP plays an important role in thermoregulation, being an endogenous antipyretic peptide (6) and playing thermoregulatory actions when injected into the central nervous system or systemically (20, 28).
However, there is only one published study (7) that evaluated the participation of AVP in hypoxia-induced anapyrexia, in which AVP does not seem to mediate the reduction in Tb. In that study, anapyrexia was similar in both Brattleboro rats (which lack AVP-containing cells in the central nervous system) and Long-Evans rats (used as a control) (7). However, thermoregulation may be aberrant in Brattleboro rats. It is known that the Brattleboro rat does not consistently develop fever in response to intraperitoneal and intracerebroventricular (icv) injections of bacterial pyrogens at doses that produce fever in normal rats (9, 14, 30). Differences could also exist regarding hypoxia-induced anapyrexia. Clearly there is a need to resolve this issue.
Thus the purpose of the present study was to examine the participation of endogenous AVP in hypoxia-induced anapyrexia by using selective AVP V1- and AVP V2-receptor blockers in Wistar rats, whose thermoregulatory mechanisms are extensively known.
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MATERIALS AND METHODS |
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Top
Abstract
Introduction
Materials and methods
Results
Discussion
References
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Animals. Experiments were performed on adult male Wistar rats that weighed 210-280 g, were housed at controlled temperature (25.2 ± 0.9°C), and were exposed to a daily 12:12-h light-dark cycle. The animals were allowed free access to water and food. Experiments were performed between 10:00 AM and 3:00 PM.
Surgery. Animals were anesthetized with 2,2,2-tribromoethanol (Aldrich, Milwaukee, WI), and a Silastic catheter was implanted through the external jugular vein according to the technique of Arms and Ojeda (1). After surgery, animals were treated with 100,000 units of benzyl-penicillin and were allowed to recover for 4 days before the experiments. During this period, the catheters were flushed daily with heparinized saline.
Rats used for icv administration were also anesthetized with 2,2,2-tribromoethanol and fixed in a stereotaxic frame. A stainless steel guide cannula (0.7-mm OD) was introduced into the third cerebral ventricle (coordinates: A,
0.4
mm; L, 0 mm;
D, 7.8-8.5 mm; Ref. 22). The
displacement of the meniscus in a water manometer assured correct
positioning of the cannula in the third ventricle. The cannula was
attached to the bone with stainless steel screws and acrylic cement. A
tight-fitting stylet was kept inside the guide cannula to prevent
occlusion. The surgical procedures were performed over a period of 40 min. Experiments were initiated 1 wk after cannula placement.
Rats used for arterial blood pressure measurements were also
anesthetized with 2,2,2-tribromoethanol (Aldrich), and a polyethylene catheter was implanted into the femoral artery for direct blood pressure recording. The arterial catheter was composed of a segment of
PE-10 tubing (4.5 cm) that was heat bonded to a 15-cm long PE-50
catheter. The catheter was filled with 0.3% heparin in sterile saline
(150 mM NaCl). The PE-10 segment was introduced into the femoral artery
until the tip reached the abdominal aorta. The catheter was secured in
position with thread, and the PE-50 segment was passed under the skin
to be finally extruded at the dorsal side of the animals. After
surgery, animals were also treated with 100,000 U of benzyl-penicillin
and were allowed to recover for 2 days before experimentation. During
this period, the catheters were flushed daily with heparinized saline.
Determination of the effect of hypoxia exposure on Tb. Rats were housed in a plastic chamber (5 liters) ventilated with humidified room air for at least 2 h. After the animals remained calm, control Tb was determined by inserting a thermoprobe into the colon. It should be pointed out that, before the experiment, the animals were habituated to temperature measurements, which were performed quickly to avoid any stress-induced elevations in Tb. Subsequently, a humidified hypoxic gas mixture of 10, 7, or 5% inspired O2 (AGA, Brazil) was flushed through the chamber for 30 min, and Tb was measured again.
Determination of the effect of AVP blockers on
Tb.
Control Tb was determined after an
initial 2-h period. Rats were then treated with
(
-mercapto-,-cyclopentamethylenepropionyl1,
O-Et-Tyr2,
Val4,
Arg8)-vasopressin (a selective
V1-receptor blocker; Sigma
Chemical, St. Louis, MO) or
(adamantaneacetyl1,
O-Et-D-Tyr2,
Val4,
Abu6,
Arg8,9)-vasopressin (a selective
V2-receptor blocker) 1 h before
Tb was measured again.
V1- and
V2-receptor blockers dissolved in pyrogen-free sterile saline were injected by intravenous (iv) bolus
injection at a dose of 10 µg/kg body weight. The dose and the period
of time after injection when Tb
was determined were chosen on the basis of previous studies (17, 18,
21, 26). The doses of both blockers were the same, because the
effective doses of these drugs are 0.49 ± 0.11 nmol/kg for the AVP
V1-receptor blocker (26) and 0.53 ± 0.07 nmol/kg for the AVP
V2-receptor blocker (18). The
volume of each injection was 0.2 ml, and the drug was flushed in with
0.3 ml of saline. Control animals received injections of saline (0.5 ml iv).
Determination of the combined effects of hypoxia and AVP blockers on Tb. The same animal chamber was used for all experiments. After the animals were habituated to the experimental condition (~2 h), control Tb was measured, and then experimental rats were treated with AVP blockers dissolved in saline at the dose of 10 µg/kg body weight by intravenous bolus injection or at the dose of 0.5 µg/kg body weight by icv injection 30 min before exposure to hypoxia. Hypoxia (7% O2) was then applied to the animals for 30 min, and Tb was measured again. Control animals received an iv (0.5 ml) or an icv (1 µl) injection of saline.
Determination of biological activity of the AVP blockers. The biological activity of the AVP V1-receptor blocker was assessed by measurements of heart rate (HR) and mean arterial blood pressure (MAP) in unanesthetized, freely moving rats; measurements were made by using a Narco polygraph (Narcotrace 80) connected to a pressure transducer (model P-10000B, Narco). A recording speed of 0.5 mm paper/s was used to minimize artifacts of blood pressure fluctuation. HR was measured by actual pulse counting at a recording speed of 5 mm paper/s. A 30-min period was initially used to measure stabilized control values of blood pressure and HR. Subsequently, animals were injected (iv) with saline, AVP V1-receptor blocker, or AVP V2-receptor blocker (10 µg/kg body weight) 1 h before AVP (0.1 µg/kg body weight) iv injection. The volume of each injection was 0.2 ml, and the drug was flushed in with 0.3 ml of saline. MAP and HR were calculated from recordings obtained 1 min after AVP injection.
The biological activity of the AVP V2-receptor blocker was assessed by measurements of urinary flow. After they were deprived of food for 14 h, the animals were weighed, and water overloads (5% of body weight, 37°C) were administered by gavage at 0 and 60 min, after which the animals were treated (iv) with AVP (1 µg/kg) combined with saline, or with AVP V1- or AVP V2-receptor blocker (10 µg/kg); then they were placed in individual metabolic cages without access to water or food. Urine samples were collected 60 min after the injections.Statistical analysis. All values are reported as means ± SD. Changes in Tb were evaluated by ANOVA. The differences between means were assessed by the Tukey-Kramer multiple-comparisons test. When variances among columns were not equal in the different groups, a nonparametric ANOVA was employed, and the difference between means was assessed by Dunn's test (see Fig. 5). Alternatively, the effect of the AVP blockers on Tb was analyzed by the paired t-test. Values of P < 0.05 were considered to be significant.
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RESULTS |
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Top
Abstract
Introduction
Materials and methods
Results
Discussion
References
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In all experimental protocols, Tb ranged from 35.9 to 37.1°C during the control period, and the baseline values of the experimental groups did not differ significantly from those of the saline group. During the experiments the mean chamber temperature was 25.2 ± 0.9°C, and room temperature was 24.3 ± 0.7°C.
Effect of hypoxia on Tb.
Figure 1 shows the effect of hypoxic
hypoxia exposure on Tb. When
inspired O2 was reduced from 21%
to 10, 7, or 5%, a significant reduction in
Tb was observed.
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Effect of the AVP V1- and AVP
V2-receptor blockers on
Tb.
No change in Tb was observed after
the AVP blockers were injected either iv or icv. These data are shown
in Table 1.
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Combined effects of hypoxia and iv injection of AVP blockers on
Tb.
Figure 2 shows the effect of hypoxia on
Tb after iv injection of saline,
AVP V1-, or AVP
V2-receptor blockers. This effect is reported as the difference between
Tb before and after hypoxia exposure (
Tb). A reduction of
1.49 ± 0.41 and 1.30 ± 0.13°C was observed in the animals
treated with the AVP V1- and AVP
V2-receptor blockers,
respectively. These values do not differ from those observed in control
animals and in animals treated with saline.
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Combined effects of hypoxia and icv injection of AVP blockers on
Tb.
Like the results shown in Fig. 2, icv injections of saline, AVP
V1- and AVP
V2-receptor blockers did not alter
the magnitude of hypoxia-induced anapyrexia. These data are plotted in
Fig. 3.
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Biological activity of the AVP blockers.
Figure 4 shows the effect of iv injection of AVP on MAP
and HR after saline, AVP V1-, or
AVP V2-receptor blocker injections iv, presented as the difference between data obtained before and after
AVP injection (HR and MAP). Control values were 110.9 ± 11.9 mmHg and 391.7 ± 21.3 beats/min for
MAP and HR, respectively. Injections of the AVP blockers caused no change in MAP or HR. AVP
injection caused a significant increase in MAP and a reduction in HR.
These effects were significantly smaller
(P < 0.05) in the animals treated
with AVP V1-receptor blocker
compared with those treated with saline.
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DISCUSSION |
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Top
Abstract
Introduction
Materials and methods
Results
Discussion
References
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The present study provides evidence that endogenous AVP does not mediate hypoxia-induced anapyrexia in rats, because neither icv nor iv treatment with AVP V1- and AVP V2-receptor blockers altered hypoxia-induced anapyrexia. Our results also show that endogenous AVP does not play any tonic role in thermoregulation under normothermic conditions.
It has been reported that AVP produces thermoregulatory actions when
injected into the central nervous system or injected systemically. AVP
injected into the ventral septal area causes antipyresis (6), and, when
injected systemically (28) or into a lateral ventricle (20), it
produces hypothermia, whereas AVP injected into the preoptic area
elicits hyperthermia (20). These data indicate that AVP exerts
thermoregulatory actions that are both neuroanatomically and
functionally specific. Moreover, Kasting (15) showed that hypertonic
saline and hemorrhage, which are potent stimuli of AVP release, cause
antipyresis in rats, indicating that endogenous AVP can affect central
febrile pathways. However, little is actually known about the
participation of endogenous AVP in thermoregulation under normothermic
conditions. In the present study, rats treated systemically and
centrally with both AVP-receptor blockers showed no change in
Tb (Table 1). This indicates that
endogenous AVP does not play a tonic role regulating temperature under
normothermic conditions. Previous studies have reported that the AVP
V1-receptor blockers
(-mercapto-,-cyclopentamethylenepropionyl1,O-Me-Tyr2,Arg8)-vasopressin
and 1-desamino-8-D-arginine
vasopressin injected into the central nervous system, do
not affect Tb (8, 19).
Several studies have investigated the biological activity of the AVP receptor blockers used in the present study (17, 18, 21, 26). In addition, we presently tested the biological activity of the AVP blockers under the same experimental conditions used to determine AVP thermoregulatory effects. AVP is classically known for its vasoconstrictor effect by interacting with the AVP V1-receptor subtype present in vascular smooth muscle and for its antidiuretic effect by interacting with the AVP V2-receptor subtype present in the distal and collector tubules of the kidneys (17). These characteristics were used to assess the biological activity of the AVP blockers. We observed that AVP injected iv caused an increase in MAP and a reduction in HR. These responses were blunted when rats were treated with the AVP V1-receptor blocker (Fig. 4). Furthermore, we also observed that AVP caused a significant reduction in urinary flow (antidiuretic effect) that was abolished by treatment with the AVP V2-receptor blocker (Fig. 5). These results indicate that the AVP receptor blockers were active and selective under the experimental conditions used in the present study.
Previous studies have demonstrated that hypoxia per se causes anapyrexia (34, 35). In addition to causing anapyrexia, hypoxia also decreases O2 consumption by a regulated inhibition of some of the processes requiring O2 (11, 25). It has been pointed out that anapyrexia is a protective response, because rats survive longer if allowed to become hypothermic during hypoxia exposure (35). Thus, anapyrexia during hypoxia offers protection mainly to O2-sensitive tissues, but the mechanisms involved remain unknown.
Candidates such as lactate (23), brain acidification (5), and histamine (13, 35) have been proposed as mediators of hypoxia-induced anapyrexia. Moreover, exclusion of glucose from central sites plays a major role in hypoglycemia-induced anapyrexia (2). A route that mediates the reduction in Tb may be the impairment of oxidative phosphorylation, because icv injection of inhibitors of oxidative phosphorylation, such as azide or cyanide, reduces the preferred Tb of toads (4). It is also known that a lack of O2 reduces oxidative phosphorylation, with a consequent increase in the intracellular levels of adenosine (35). Because adenosine reduces Tb (32), it could be a mediator of hypoxia-induced anapyrexia. Furthermore, it is also possible that hypoxia elicits anapyrexia through a direct effect on thermosensitive neurons in the preoptic area of the anterior hypothalamus (29).
AVP has also been extensively suggested as a mediator of hypoxia-induced anapyrexia. Rationales for this hypothesis are 1) hypoxia increases AVP levels in plasma and cerebrospinal fluid (10, 24); 2) AVP injected icv (20) or systemically (28) elicits anapyrexia in rats; 3) water deprivation is known to increase AVP levels in plasma and cerebrospinal fluid in response to increased extracellular tonicity and diminished plasma volume in mammals (31); the toad Bufo marinus selects significantly lower preference temperatures when exposed to dry air (16), and camels reduce their metabolic rate when hypohydrated (27); and 4) Shido et al. (28) demonstrated that peripheral vasopressin-induced anapyrexia is attributed to the suppression of nonshivering thermogenesis, and it is known that hypoxia elicits anapyrexia by inhibiting thermogenesis (35). However, the present study does not support this hypothesis, because neither icv nor iv treatment with AVP blockers altered the magnitude of the drop in Tb after exposure to hypoxia (Figs. 2 and 3).
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ACKNOWLEDGEMENTS |
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We acknowledge the excellent technical assistance of Mauro F. Silva and Andréia F. C. Leone.
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FOOTNOTES |
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This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) and Conselho Nacional de Desenvolvimento Científico e Tecnológico. A. A. Steiner was the recipient of a FAPESP undergraduate fellowship.
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: L. G. S. Branco, Departamento de Fisiologia, Faculdade de Odontologia de Ribeirão Preto/USP, 14040-904 Ribeirão Preto, São Paulo, Brazil (E-mail: lgsbranc{at}usp.br).
Received 23 June 1998; accepted in final form 5 October 1998.
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References
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