Drop In Tb Research Articles

Experimental studies of strong dipolar interparticle interaction in monodisperse Fe3O4 nanoparticles

Interparticle interaction of monodisperse Fe3O4 nanoparticles has been experimentally investigated by dispersing the nanoparticles in solvents. With increasing the interparticle distances to larger than 100nm in a controlled manner, the authors found that the blocking temperature (TB) of the nanoparticles drops continuously and eventually gets saturated with a total drop in TB of 7–17K observed for 3, 5, and 7nm samples, compared with their respective nanopowder samples. By carefully studying the dependence of TB on the interparticle distance, the authors could demonstrate that the experimental dependence of TB follows the theoretical curve of the dipole-dipole interaction.

NNOS is involved in behavioral thermoregulation of newborn rats during hypoxia

The present study was undertaken to investigate the role of nitric oxide (NO) pathway in the behavioral thermoregulation of newborn rats in cold and hypoxia. We predicted that injection of l-NAME (non-selective NO synthase (NOS) inhibitor) and SMTC (neuronal NOS (nNOS) inhibitor) would restore the huddling behavior and eliminate the reduction of Tb caused by hypoxia. Experiments were performed on Wistar rat pups of 7–9 days old. We measured Tb and analyzed the huddling behavior by means of the calculation of the total surface area occupied by 5 pups and the number of single pups grouped in the center of a chamber at 20 °C, before and after l-NAME, SMTC or their respective vehicles ( d-NAME and saline) s.c. injections. Subsequently, the pups were exposed to hypoxia (10% O 2) during 30 min, whereas control animals were kept under normoxia. The experiments were monitored by a digital camera. All animals were hypothermic when exposed to 20 °C. There was no significant difference in Tb, total area and number of single pups in normoxia after treatments. During hypoxia, the drop in Tb was higher in control groups, and this effect was attenuated by l-NAME and SMTC injections. Hypoxia increased the area occupied by the pups in saline, d-NAME and l-NAME groups, while SMTC attenuated this response. The data indicate that NO pathway is involved in the inhibition of huddling behavior and in the reduction of Tb caused by hypoxia, but plays no role during normoxia. Furthermore, NO seems to arise from the nNOS isoform.

The importance of diurnal processes for the Seasonal cycle of Sea-ice microwave brightness temperatures during early Summer in the Weddell Sea, Antarctica

AbstractOver the perennial Sea ice in the western and central Weddell Sea, Antarctica, the onset of Summer is accompanied by a Significant decrease of Sea-ice brightness temperatures (Tb) as observed by passive-microwave radiometers Such as the Special Sensor Microwave/Imager (SSM/I). The Summer-specific Tbdrop is the dominant feature in the seasonal cycle of Tbdata and represents a conspicuous difference to most Arctic Sea-ice regions, where the onset of Summer is mostly marked by a rise in Tb. Data from a 5 week drift Station through the western Weddell Sea in the 2004/05 austral Summer, Ice Station POLarstern (IsPOL), helped with identifying the characteristic processes for Antarctic Sea ice. In Situ glaciological and meteorological data, in combination with SSM/I Swath Satellite data, indicate that the cycle of repeated diurnal thawing and refreezing of Snow (‘freeze–thaw cycles’) is the dominant process in the Summer Season, with the absence of complete Snow wetting. The resulting metamorphous Snow with increased grain Size, as well as the formation of ice layers, leads to decreasing emissivity, enhanced volume Scattering and increased backscatter. This causes the Summer Tbdrop.

Respiratory and body temperature modulation by adenosine A1 receptors in the anteroventral preoptic region during normoxia and hypoxia

The present study was undertaken to investigate adenosine as a simultaneous mediator of hypoxia-induced hyperventilation and regulated hypothermia in the anteroventral preoptic region (AVPO), the thermointegrative region of the central nervous system (CNS). Accordingly, we predicted that injection of aminophylline and DPCPX, non-selective and A(1) receptor antagonists, respectively, into the AVPO would exacerbate the ventilatory response and lessen the drop in body temperature (T(b)) caused by hypoxia. We measured ventilation (V ) and T(b) of conscious Wistar rats before and after AVPO injection of aminophylline (1 and 10 microg/100 nL) or DPCPX (17.5 and 175 ng/100 nL), or their respective vehicles, followed by 30 min of hypoxia (7% O(2)). Vehicles and the lower doses of both antagonists had no effect on V and T(b) during normoxia or hypoxia. The higher doses of aminophylline and DPCPX increased (P<0.05) the hypoxia-induced hyperventilation, whereas the drop in T(b) elicited by hypoxia was attenuated (P<00.05) by DPCPX only. This higher DPCPX dose also increased T(b) during normoxia. The present data is consistent with the notion that adenosine plays an inhibitory role in respiratory and metabolic regulation, in a way that A(1) receptors stimulation in the AVPO inhibits ventilatory drive during hypoxia and tonically modulates basal T(b).

Involvement of serotoninergic receptors in the anteroventral preoptic region on hypoxia-induced hypothermia

Hypoxia causes a regulated decrease in body temperature (Tb). There is circumstantial evidence that the neurotransmitter serotonin (5-HT) in the anteroventral preoptic region (AVPO) mediates this response. However, which 5-HT receptor(s) is (are) involved in this response has not been assessed. Thus, we investigated the participation of the 5-HT receptors (5-HT 1, 5-HT 2, and 5-HT 7) in the AVPO in hypoxic hypothermia. To this end, Tb of conscious Wistar rats was monitored by biotelemetry before and after intra-AVPO microinjection of methysergide (a 5-HT 1 and 5-HT 2 receptor antagonist, 0.2 and 2 μg/100 nL), WAY-100635 (a 5-HT 1A receptor antagonist, 0.3 and 3 μg/100 nL), and SB-269970 (a 5-HT 7 receptor antagonist, 0.4 and 4 μ/100 nL), followed by 60 min of hypoxia exposure (7% O 2). During the experiments, the mean chamber temperature was 24.6 ± 0.7 °C (mean ± SE) and the mean room temperature was 23.5 ± 0.8 °C (mean ± SE). Intra-AVPO microinjection of vehicle or 5-HT antagonists did not change Tb during normoxic conditions. Exposure of rats to 7% of inspired oxygen evoked typical hypoxia-induced hypothermia after vehicle microinjection, which was not affected by both doses of methysergide. However, WAY-100635 and SB-269970 treatment attenuated the drop in Tb in response to hypoxia. The effect was more pronounced with the 5-HT 7 antagonist since both doses (0.4 and 4 μg/0.1μL) were capable of attenuating the hypothermic response. As to the 5-HT 1A antagonist, the attenuation of hypoxia-induced hypothermia was only observed at the higher dose. Therefore, the present results are consistent with the notion that 5-HT acts on both 5-HT 1A and 5-HT 7 receptors in the AVPO to induce hypothermia, during hypoxia.

Evidence for thermoregulation by dopamine D1 and D2 receptors in the anteroventral preoptic region during normoxia and hypoxia

Hypoxia causes a regulated decrease in body temperature (Tb), a response that has been called anapyrexia. Stimulation of dopamine receptors in the central nervous system (CNS) reduces Tb in rats, and dopamine D1 and D2 receptors seem to be involved in this response. Thus, we predicted that injection of SCH 23390 and haloperidol, D1 and partly D2 receptor antagonists, respectively, into the anteroventral preoptic region (AVPO, the thermointegrative region of the CNS) would lessen the hypoxia-induced anapyrexia. We measured Tb of conscious Wistar rats before and after injection of SCH 23390 (50 and 100 ng/100 nl) or haloperidol (50 e 500 ng/100 nl) or their respective vehicles (saline and DMSO 5%) into the AVPO followed by 30 min of hypoxia (7% O 2). Vehicles and the lower doses of SCH 23390 and haloperidol had no effect on Tb during normoxia or hypoxia. The higher doses of SCH 23390 and haloperidol attenuated ( P<0.05) the drop in Tb elicited by hypoxia. However, this higher haloperidol dose also increased Tb during normoxia. The present data is consistent with the notion that dopamine is an important thermoregulatory neurotransmitter in a way that D2 receptors are mainly involved with maintenance of Tb in euthermia, while D1 receptors are activated to induce hypoxic anapyrexia in the AVPO.

Glutamatergic neurotransmission modulates hypoxia-induced hyperventilation but not anapyrexia.

The interaction between pulmonary ventilation (V E) and body temperature (Tb) is essential for O2 delivery to match metabolic rate under varying states of metabolic demand. Hypoxia causes hyperventilation and anapyrexia (a regulated drop in Tb), but the neurotransmitters responsible for this interaction are not well known. Since L-glutamate is released centrally in response to peripheral chemoreceptor stimulation and glutamatergic receptors are spread in the central nervous system we tested the hypothesis that central L-glutamate mediates the ventilatory and thermal responses to hypoxia. We measured V E and Tb in 40 adult male Wistar rats (270 to 300 g) before and after intracerebroventricular injection of kynurenic acid (KYN, an ionotropic glutamatergic receptor antagonist), alpha-methyl-4-carboxyphenylglycine (MCPG, a metabotropic glutamatergic receptor antagonist) or vehicle (saline), followed by a 1-h period of hypoxia (7% inspired O2) or normoxia (humidified room air). Under normoxia, KYN (N = 5) or MCPG (N = 8) treatment did not affect V E or Tb compared to saline (N = 6). KYN and MCPG injection caused a decrease in hypoxia-induced hyperventilation (595 +/- 49 for KYN, N = 7 and 525 +/- 84 ml kg-1 min-1 for MCPG, N = 6; P < 0.05) but did not affect anapyrexia (35.3 +/- 0.2 for KYN and 34.7 +/- 0.4 masculine C for MCPG) compared to saline (912 +/- 110 ml kg-1 min-1 and 34.8 +/- 0.2 masculine C, N = 8). We conclude that glutamatergic receptors are involved in hypoxic hyperventilation but do not affect anapyrexia, indicating that L-glutamate is not a common mediator of this interaction.

Determination of temperature preference and the role of the enlarged cheliped in thermoregulation in male sand fiddler crabs, Uca pugilator

1.Male Uca pugilator whose major cheliped was immersed in 3°C water bath experienced a significant drop in Tb. Thus, the enlarged claw of male Uca pugilator may have an unexplored function: thermoregulation.2.Crabs prefer warmer substrates (19–24 and 28–30°C) over cooler (15–17°C).3.Mean selected temperature (MST) may not be an accurate reflection of Tb. Crabs in a thermal chamber preferred temperatures between 25 and 30°C but their average Tb was 23.2°C.

Regulation of breathing and body temperature of a burrowing rodent during hypoxic?hypercapnia

Burrowing mammals usually have low respiratory sensitivity to hypoxia and hypercapnia. However, the interaction between ventilation (V), metabolism and body temperature (Tb) during hypoxic–hypercapnia has never been addressed. We tested the hypothesis that Clyomys bishopi, a burrowing rodent of the Brazilian cerrado, shows a small ventilatory response to hypoxic–hypercapnia, accompanied by a marked drop in Tb and metabolism. V, Tb and O2 consumption (V̇O2) of C. bishopi were measured during exposure to air, hypoxia (10% and 7% O2), hypercapnia (3% and 5% CO2) and hypoxic–hypercapnia (10% O2+ 3% CO2). Hypoxia of 7% but not 10%, caused a significant increase in V, and a significant drop in Tb. Both hypoxic levels decreased V̇O2 and 7% O2 significantly increased V/V̇O2. Hypercapnia of 5%, but not 3%, elicited a significant increase in V, although no significant change in Tb, V̇O2 or V/V̇O2 was detected. A combination of 10% O2 and 3% CO2 had minor effects on V and Tb, while V̇O2 decreased and V/V̇O2 tended to increase. We conclude that C. bishopi has a low sensitivity not only to hypoxia and hypercapnia, but also to hypoxic–hypercapnia, manifested by a biphasic ventilatory response, a drop in metabolism and a tendency to increase V/V̇O2. The effect of hypoxic–hypercapnia was the summation of the hypoxia and hypercapnia effects, with respiratory responses tending to have hypercapnic patterns while metabolic responses, hypoxic patterns.

Regulation of breathing and body temperature of a burrowing rodent during hypoxic–hypercapnia

Burrowing mammals usually have low respiratory sensitivity to hypoxia and hypercapnia. However, the interaction between ventilation ( V), metabolism and body temperature (Tb) during hypoxic–hypercapnia has never been addressed. We tested the hypothesis that Clyomys bishopi, a burrowing rodent of the Brazilian cerrado, shows a small ventilatory response to hypoxic–hypercapnia, accompanied by a marked drop in Tb and metabolism. V, Tb and O 2 consumption (V̇O 2) of C. bishopi were measured during exposure to air, hypoxia (10% and 7% O 2), hypercapnia (3% and 5% CO 2) and hypoxic–hypercapnia (10% O 2+ 3% CO 2). Hypoxia of 7% but not 10%, caused a significant increase in V, and a significant drop in Tb. Both hypoxic levels decreased V̇O 2 and 7% O 2 significantly increased V/V̇O 2. Hypercapnia of 5%, but not 3%, elicited a significant increase in V, although no significant change in Tb, V̇O 2 or V/V̇O 2 was detected. A combination of 10% O 2 and 3% CO 2 had minor effects on V and Tb, while V̇O 2 decreased and V/V̇O 2 tended to increase. We conclude that C. bishopi has a low sensitivity not only to hypoxia and hypercapnia, but also to hypoxic–hypercapnia, manifested by a biphasic ventilatory response, a drop in metabolism and a tendency to increase V/V̇O 2. The effect of hypoxic–hypercapnia was the summation of the hypoxia and hypercapnia effects, with respiratory responses tending to have hypercapnic patterns while metabolic responses, hypoxic patterns.

Central dopamine modulates anapyrexia but not hyperventilation induced by hypoxia.

Hypoxia causes hyperventilation and decreases body temperature (T(b)) and metabolism [O(2) consumption (VO(2))]. Because dopamine (DA) is released centrally in response to peripheral chemoreceptor stimulation, we tested the hypothesis that central DA mediates the ventilatory, thermal, and metabolic responses to hypoxia. Thus we predicted that injection of haloperidol (a DA D(2)-receptor antagonist) into the third ventricle would augment hyperventilation and attenuate the drop in T(b) and VO(2) in conscious rats. We measured ventilation, T(b), and VO(2) before and after intracerebroventricular injection of haloperidol or vehicle (5% DMSO in saline), followed by a 30-min period of hypoxia exposure. Haloperidol did not change T(b) or VO(2) during normoxia; however, breathing frequency was decreased. During hypoxia, haloperidol significantly attenuated the falls in T(b) and VO(2), although hyperventilation persisted. The present study shows that central DA participates in the thermal and metabolic responses to hypoxia without affecting hyperventilation, showing that DA is not a common mediator of this interaction.

An edge detection technique to estimate melt duration, season and melt extent on the Greenland Ice Sheet using Passive Microwave Data

The melt extent, duration and melt season on the Greenland ice sheet were estimated using an edge detection technique on passive microwave data from the SSM/I and SMMR instruments (18/19V GHz channel) for the period 1979 to 1997. The annual brightness temperature (Tb) time series at a pixel location that experiences summer melt has a steep rise and drop in Tb with the onset and end of melt, respectively. A derivative‐of‐Gaussian edge detector is used to detect edges corresponding to the onset and end of melt. The time lapsed between the first upward and last downward edge on the annual Tb time series gives an estimate of the melt season and the time lapsed between successive upward and downward edges gives the duration of melt. While the maximum melt extent increased by 18%, the total duration of melt increased by 3.7% and the total melt season decreased by 3.8% during the period 1979–1997.

Role of nitric oxide in thermoregulation and hypoxic ventilatory response in obese Zucker rats.

To examine the role of nitric oxide (NO) on thermoregulation and control of breathing in obesity, awake obese and age-matched lean Zucker (Z) rats underwent a sustained hypoxic challenge. Body temperature (Tb), oxygen consumption (V O(2)) and ventilation (V E) were measured during room air and during 30-min of hypoxia (10% O(2)) after intraperitoneal administration of either 100 mg/kg of N(G)-nitro-L-arginine methyl ester (L-NAME), a nonspecific NOS inhibitor, 25 mg/kg of 7-nitroindazole (7-NI), a selective neuronal NOS inhibitor, or equal volume of vehicle (dimethyl sulfoxide: DMSO) as control. Tb in obese rats during room air was significantly lower than that of lean rats. Hypoxia induced a more pronounced drop in Tb and V O(2) in lean rats than in obese rats. Tb in lean Z rats dropped significantly by approximately 0.2 degrees C after L-NAME and, more markedly, by approximately 1.1 degrees C after 7-NI compared with control during room air, whereas Tb in obese Z rats was unaffected. L-NAME and 7-NI attenuated hypoxia-induced hypothermia or hypometabolism in lean rats, but not in obese rats. Lean rats exhibited an abrupt increase in V E in response to hypoxia followed by a gradual decline in V E. In contrast, obese rats displayed an initial increase in V E that plateaued during sustained hypoxia. Both L-NAME and 7-NI induced marked decreases in V E during room air and hypoxia compared with control lean rats, whereas V E was virtually unaffected by either agent in obese rats. The present results suggest that the blunted thermoregulatory and ventilatory responses to hypoxia in obese Z rats may be attributed to reduced activity of NOS in the central nervous system.

EXERCISE DELAYS THE HYPOXIC-HYPOTHERMIC RESPONSE

Exercise during the initial exposure to high altitude results in an exacerbation of acute mountain sickness in humans. The mechanism responsible remains unknown. Sustained exposure to hypoxia results in an initial decrease in body temperature (Tb) followed by a return to baseline in rats. The initial drop in Tb may be neuro-protective. We hypothesized that exercise during the initial phase of hypoxia would counteract the hypoxic-hypothermic response (HHR). Male Sprague-Dawley rats were divided into exercise (EX, n = 6) or sedentary groups (SED, n = 4). Tb was measured with implanted Mini-mitter telemetry probes. Animals underwent a 24 hour control (normaoxia) period, followed by a 24 hour hypoxia (10% O2) period at an ambient T of 25 °C. During the initial 6 hours of hypoxia, EX animals walked (10m/min) on a treadmill (30min on/30 min off), followed by 18 hours of rest. SED animals were exposed to 24 hours of hypoxia with no exercise. During the initial 6 hours of hypoxia, Tb in SED animals decreased compared to baseline (38.2 ± 0.1 (SD) vs. 36.1 ± 1.1 °C, P = .027), whereas no change was observed in the EX animals (37.6 ± 0.1 vs. 37.6 ± 1.3 °C). Following the cessation of exercise, Tb decreased in EX animals and reached a similar nadir in Tb as SED animals (34.8 ± 1.6 vs. 34.8 ± 0.6 °C, respectively). Thus, the time to attain the Tb nadir following hypoxia exposure was significantly longer in EX compared to SED animals (10.9 ± 1.4 vs. 5.9 ± 2.2 hours respectively, P = .002). We conclude that exercise during the initial exposure to hypoxia in rats delays, but does not prevent, the HHR. Whether the exercise delay in lowering Tb is sufficient to cause more pronounced neuro-pathology remains to be determined. Supported by the American Lung Association of New York.

Effects of hypoxia and hypothermia on the end-inspiratory pause and Hering-Breüer reflex in the neonatal tammar wallaby

When cooled in normoxia newborn rats decreased body temperature (Tb), increased metabolic rate and weakened the intensity of the vagally mediated Hering-Breuer inspiratory inhibition reflex (HB reflex) [1]. On the other hand cooling in hypoxia decreased both Tb and metabolic rate and had no effect on HB reflex intensity [2]. This suggested that in newborn rats the effect of cooling on the strength of the HB reflex was not attributable to Tb per se but to the corresponding changes in metabolic rate [2]. Nevertheless, in normoxia the drop in Tb with cooling, via the Q10 effect, could oppose the changes in metabolic rate induced by thermogenesis, and the hypoxia per se could be expected to provide a 'drive' through its effect on the peripheral chemoreceptors. To clarify the effects of hypothermia and hypoxia on the HB reflex in the absence of thermogenesis we examined the ectothermic neonatal tammar wallaby (Macropus eugenii). As newborn marsupials breathe with a pronounced end-inspiratory pause [3,4], the result of vagally controlled laryngeal closure [3], the effect of cooling and hypoxia on the end-inspiratory pause was also examined. Neonates (aged 2–3 weeks, mass ~2.5 g) were studied at Tb of 36.5 (normothermia), 32, 28 and 20°C in normoxia or hypoxia (10% O2). The rate of oxygen consumption (VO2), breathing pattern and ventilation (??E) were measured as previously described [4]. Applying a vacuum across the body until the first inspiratory effort induced the HB reflex, quantified as the inhibitory ratio (IR) of the expiratory time during lung inflation compared to the expiratory time during spontaneous breathing (TE). At 36.5°C in normoxia the tammar neonate exhibited a marked IR to maintained lung inflations at -5 and -10 cm H2O. Acute hypoxia invoked a hyperpnea (+42%) and hypometabolism (-30%) and reduced the IR by ~50% at -10 cm H2O and abolished it at -5 cm H2O. This is in agreement with the effects of hypoxia on hyperventilation and the HB reflex in 8-day-old rat pups [5] which possess a greater chemosensitivity than newborn rats. In normoxia decreased Tb was associated with a decrease in VO2 yet ??E/VO2 remainedunchanged (~32) to that at 36.5°C; the decrease in ??E was contributed to by an increase in TE, primarily the end-inspiratory pause. Associated with the increase in expiratory time was a failure to elicit a HB reflex at either -5 or -10 cm H2O. At lower temperatures exposure to hypoxia maintained the hyperventilation (??E/VO2 ~62) seen at 36.5°C, though at these temperatures this was achieved solely through a hypometabolic response. Whether the lack of hyperpneic response was affected by the affect of hypothermia on chemo-afferents [6] is unknown but maintenance of ??E/VO2 during hypothermia in the 2–3 week old tammar wallaby suggests that, relative to metabolic rate, respiratory gain, which is centrally controlled, is not depressed. Additionally, hypothermia prolongs the end-inspiratory pause presumably through temperature effects on neural function [7] and that these appear to predominate the vagally mediated HB reflex.

Role of nitric oxide in hypoxia inhibition of fever

Hypoxia causes a regulated decrease in body temperature (T(b)), and nitric oxide (NO) is now known to participate in hypoxia-induced hypothermia. Hypoxia also inhibits lipopolysaccharide (LPS)-induced fever. We tested the hypothesis that NO may participate in the hypoxia inhibition of fever. The rectal temperature of awake, unrestrained rats was measured before and after injection of LPS, with or without concomitant exposure to hypoxia, in an experimental group treated with N(omega)-nitro-L-arginine (L-NNA) for 4 consecutive days before the experiment and in a saline-treated group (control). L-NNA is a nonspecific NO synthase inhibitor that blocks NO production. LPS caused a dose-dependent typical biphasic rise in T(b) that was completely prevented by hypoxia (7% inspired oxygen). L-NNA caused a significant drop in T(b) during days 2-4 of treatment. When LPS was injected into L-NNA-treated rats, inhibition of fever was observed. Moreover, the effect of hypoxia during fever was significantly reduced. The data indicate that the NO pathway plays a role in hypoxia inhibition of fever.

Ventilatory response to asphyxia in conscious rats: effect of ambient and body temperatures

In many mammals the ventilatory response to hypoxia depends on ambient temperature (Ta), largely because of the hypometabolic effects of hypoxia below thermoneutrality. We questioned whether the ventilatory response to asphyxia also depends upon Ta, and the role played by metabolism and body temperature (Tb). Oxygen consumption ( V ̇ O 2 ) and pulmonary ventilation (V̇ e) were measured in conscious rats at Ta=27°C (warm) and 11°C (cold), breathing air or two levels of asphyxic gases, moderate (10% O 2–4% CO 2), or severe (10% O 2–8% CO 2), for ≈30 min each. In the cold, the pattern of the V̇ e response to moderate asphyxia was qualitatively similar to that seen in hypoxia alone, i.e the attained V ̇ e / V ̇ O 2 was similar in warm and cold conditions, with, in the latter, a major drop in V ̇ O 2 and little or no hyperpnea. During severe asphyxia, however, the V ̇ e / V ̇ O 2 attained in the cold was less than in the warm, and it was accompanied by a large drop in Tb (≈6°C). Blood gases confirmed the lower asphyxic hyperventilation in the cold. By maintaining Tb at 38°C with an implanted abdominal heat exchanger, the V ̇ e / V ̇ O 2 levels attained during asphyxia were the same between cold and warm conditions. We conclude that (a) the V̇ e response to asphyxia is Ta-dependent, largely because of the hypometabolic effect of the hypoxic component in the cold, (b) during moderate asphyxia the hypercapnic component is qualitatively unimportant, and (c) with severe asphyxia the hypercapnia becomes an important contributor to the Ta-sensitivity by aggravating the decrease in Tb in the cold and lowering V̇ e sensitivity.

Phentolamine and thermoregulation in rats

Phentolamine (PHEN), a nonselective alpha-adrenoceptor antagonist, causes a dose and ambient temperature (Ta)-dependent fall in body temperature (Tb) when injected intraperitoneally. In this paper, we investigated whether this was caused by integrated behavioral and autonomic thermoregulatory responses and whether it was due to a central action of the drug. Male rats were trained to press a bar for warm air in the cold or cold air in the heat. Rats were tested in both conditions near their Tb peaks and troughs after injections of saline or PHEN (5 and 10 mg/kg, IP). Tb fell significantly within the first 30 min post-PHEN, and after that, in the cold, the rats worked to increase Ta. In the heat they did not change Ta. To determine what was responsible for the Tb fall, we measured heat loss and heat production after saline or PHEN (10 mg/kg; IP) at Ta 2, 20, and 30 degrees C. Decreases in Tb at 2 and 20 degrees C were caused by increased heat loss during the first 15-30 min post-PHEN. At 2 degrees C, heat production increased after the drop in Tb. We conclude that the main reason the rats do not start to work immediately to prevent their core temperature from falling is that skin temperature is high, due to peripheral vasodilation, and that skin temperature is the major stimulus for regulating preferred Ta. We believe these effects are mediated by peripheral mechanisms because intracerebro-ventricular injections of PHEN did not cause a fall in Tb.

Nocturnal Hypothermia in Gray Jays Perisoreus canadensis Wintering in Interior Alaska

Radio-telemetry measurements were made of deep body temperature (Tb) in winter acclimatized Gray Jays Perisoreus canadensis held in an outdoor aviary at 66040'N, 150'33'W between 3 December 1987 and 29 January 1988. The diurnal rhythm of Tb was similar among the three individuals tested. Upon roosting for the night, the birds experienced a gradual drop in Tb until about 0500-0700 hours. Tb then levelled off until approximately 0800 when it began to rise sharply to the usual daytime level just before the birds became active. In contrast to a previous study which failed to demonstrate any appreciable nocturnal hypothermic response in a winter-acclimatized Gray Jay, the birds tested in the present study dropped their body temperature at night substantially (range: 4.5 6.1?C) below their mean daytime temperature of approximately 42'C. Moreover, the extent of the hypothermic response was correlated with the minimum overnight air temperature; on colder nights the jays tended to drop their body temperature to a greater extent. These results suggest that Gray Jays may save appreciable amounts of energy during the long, cold nights of the arctic winter as a result of their hypothermic response.

The Cost of Burrowing by the Social Mole Rats (Bathyergidae) Cryptomys damarensis and Heterocephalus glaber: The Role of Soil Moisture

The cost of burrowing (oxygen consumption) was compared between two social mole rats, Cryptomys damarensis and Heterocephalus glaber, in damp and dry sand. Cryptomys damarensis had a digging metabolic rate (DMR) of 2.86 ± 0.31 cm³ · g⁻¹ · h⁻¹ in damp sand and of 2.58 ± 0.32 cm³ · g⁻¹ · h⁻¹ in dry sand. The DMR was 4.53-5.03 times the resting metabolic rate (RMR). Its burrowing speed was 3.53 ± 0.75m · h⁻¹ in damp sand and 0.92 ± 0.33m · h⁻¹ in dry sand. Body temperature Tb increased by 1.3° C during burrowing in dry sand. Heterocephalus glaber had a DMR of 3.36 ± 0.25 cm³ · g⁻¹ · h⁻¹ in damp sand and of 2.78 ± 0.25 cm³ · g⁻¹ · h⁻¹ in dry sand. The DMR was 4.34–5.25 times RMR. Its burrowing speed was 0.75 ± 0.23 m · h⁻¹ in damp sand and 0.30 ± 0.02 m · h⁻¹ in dry sand. There was a 2.3° C drop in Tb during burrowing in damp sand. For both species, the cost of burrowing was 1.5–3.7 times greater in dry sand than in damp sand. These data are compared with those of other subterranean mammals. Arguments are presented that suggest that the cost of burrowing may be an important factor selecting for body size, differentiation of labor, and polyethism in the bathyergids.