Thermal Tachypnea Research Articles

Cutaneous TRPV4 Channels Activate Warmth-Defense Responses in Young and Adult Birds.

Transient receptor potential vanilloid 4 (TRPV4) channels are sensitive to warm ambient temperatures (Tas), triggering heat loss responses in adult rats in a Tas range of ∼26–30°C. In birds, however, the thermoregulatory role of TRPV4 has never been shown. Here, we hypothesized that stimulation of TRPV4 induces thermolytic responses for body temperature (Tb) maintenance in birds, and that this function is already present in early life, when the Ta range for TRPV4 activation does not represent a warm condition for these animals. We first demonstrated the presence of TRPV4 in the dorsal and ventral skin of chickens (Gallus gallus domesticus) by immunohistochemistry. Then, we evaluated the effects of the TRPV4 agonist, RN1747, and the TRPV4 antagonists, HC067047 and GSK2193874, on Tb and thermoeffectors at different Tas in 5-day-old chicks and 60-day-old adult chickens. For the chicks, RN1747 transiently reduced Tb both in thermoneutrality (31°C) and in a cold Ta for this phase (26°C), which relied on huddling behavior inhibition. The TRPV4 antagonists alone did not affect Tb or thermoeffectors but blocked the Tb decrease and huddling inhibition promoted by RN1747. For the adults, TRPV4 antagonism increased Tb when animals were exposed to 28°C (suprathermoneutral condition for adults), but not to 19°C. In contrast, RN1747 decreased Tb by reducing metabolic rate and activating thermal tachypnea at 19°C, a Ta below the activation range of TRPV4. Our results indicate that peripheral TRPV4 receptors are functional in early life, but may be inhibited at that time when the range of activation (∼26–30°C) represents cold Ta for chicks, and become physiologically relevant for Tb maintenance when the activation Ta range for TRPV4 becomes suprathermoneutral for adult chickens.

A thermoregulatory role of the medullary raphe in birds.

The brainstem region medullary raphe modulates non-shivering and shivering thermogenesis and cutaneous vasomotion in rodents. Whether the same scenario occurs in the other endothermic group, i.e. birds, is still unknown. Therefore, we hypothesised that the medullary raphe modulates heat gain and loss thermoeffectors in birds. We investigated the effect of glutamatergic and GABAergic inhibitions in this specific region on body temperature (Tb), oxygen consumption (thermogenesis), ventilation (O2 supply in cold, thermal tachypnea in heat) and heat loss index (cutaneous vasomotion) in one-week-old chicken exposed to neutral (31°C), cold (26°C) and heat (36°C) conditions. Intra-medullary raphe antagonism of NMDA glutamate (AP5; 0.5, 5 mM) and GABAA (bicuculline; 0.05, 0.5 mM) receptors reduced Tb of chicks at 31°C and 26oC, due mainly to an O2 consumption decrease. AP5 transiently increased breathing frequency during cold exposure. At 31°C, heat loss index was higher in the bicuculline and AP5 groups (higher doses) than vehicle at the beginning of the Tb reduction. No treatment affected any variable tested at 36oC. The results suggest that glutamatergic and GABAergic excitatory influences on the medullary raphe of chicks modulate thermogenesis and glutamatergic stimulation prevents tachypnea, without having any role in warmth-defence responses. A double excitation influence on the medullary raphe may provide a protective neural mechanism for supporting thermogenesis during early life, when energy expenditure to support growth and homeothermy is high. This novel demonstration of a thermoregulatory role for the raphe in birds suggests a convergent brainstem neurochemical regulation of body temperature in endotherms.

Thermal tachypnea in avian embryos.

Many adult mammals and birds respond to high surrounding temperatures with thermal tachypnea - an increase in breathing frequency accompanied by shallow tidal volume, with minimal increase in oxygen consumption (V̇O2 ). This pattern favors heat dissipation by evaporative water loss (EWL) through the respiratory tract. We asked to what extent this response was apparent at the earliest stages of development, when pulmonary ventilation initiates. Measurements of pulmonary ventilation (V̇E; barometric technique), V̇O2 (open-flow methodology) and EWL (water scrubbers) were performed on chicken embryos at the earliest appearance of pulmonary ventilation, during the internal pipping stage. Data were collected, first, at the normal incubation temperature (37.5°C); then, ambient and egg temperatures were increased to approximately 44°C over a 2 h period. Other embryos of the same developmental stage (controls) were maintained in normothermia for the whole duration of the experiment. During heat exposure, the embryo's V̇O2 and carbon dioxide production increased little. In contrast, V̇E more than doubled (∼128% increase), entirely because of the large rise in breathing frequency (∼132% increase), with no change in tidal volume. EWL did not change significantly, probably because, within the egg, the thermal and water vapor gradients are almost nonexistent. We conclude that chicken embryos respond to a major heat load with tachypnea, like many adult mammals and birds do. Its appearance so early in development, although ineffective for heat loss, signifies that thermal tachypnea represents an important breathing response necessary to be functional from hatching.

Changes in lung surfactant proteins in rats with lipopolysaccharide-induced fever.

The study was designed to prove the hypothesis that lipopolysaccharide (LPS)-induced fever elicits the changes in surfactant specific proteins, potentially related to thermal tachypnea. In adult rats fever was induced by intraperitoneal administration of LPS at a dose 100 microg/kg of body weight; control group received saline. Respiratory parameters, arterial blood gases and pH and colonic body temperature (BT) were recorded. Five hours later, surfactant proteins (SP) A, B, C and D were evaluated in bronchoalveolar lavage fluid (BALF) and lung tissue (LT). LPS evoked monophasic thermic response (at 300 min 38.7+/-0.2 vs. 36.4+/-0.3 °C, P 0.05) and an increase in minute ventilation due to changes in breathing rate and tidal volume. LPS-instilled animals had higher levels of SP-A and SP-D in LT (P 0.05 and 0.01), and higher SP-D in BALF (P 0.01) than controls. SP-B increased in LT and SP-C in BALF of animals with LPS (both P 0.05 vs. controls). The changes in all surfactant specific proteins are present in LPS-induced fever. Alterations of proteins related to local immune mechanisms (SP-A, SP-D) are probably a part of general inflammatory response to pyrogen. Changes in proteins related to surface activity (SP-B and SP-C) might reflect the effort of the body to stabilize the lungs in thermal challenge.

Evaporative heat loss in Bos taurus: Do different cattle breeds cope with heat stress in the same way?

The aim of this study was to compare two Portuguese (Alentejana and Mertolenga) and two exotic (Frisian and Limousine) cattle breeds in terms of the relationship between the increase in ambient temperature and the responses of the evaporative heat loss pathways and the effects on homeothermy. In the experiment, six heifers of the Alentejana, Frisian, and Mertolenga breeds and four heifers of the Limousine breed were used. The animals were placed in four temperature levels, the first one under thermoneutral conditions and the other ones with increase levels of thermal stress. When submitted to severe heat stress, the Frisian developed high thermal tachypnea (125mov/min) and moderate sweating rates (117gm−2h−1), which did not prevent an increase in the rectal temperature (from 38.4°C to 40.0°C). Moderate increases in rectal temperature were observed in the Alentejana (from 38.8°C to 39.4°C) and Limousine (from 38.6°C to 39.4°C), especially in the period of highest heat stress. The Limousine showed moderate levels of tachypnea (101mov/min) while showing the lowest sweating rates. The Alentejana showed significant increases in sweating rate (156gm−2h−1) that played a major role in homeothermy. The Mertolenga showed a superior stability of body temperature, even in the period of highest heat stress (from 38.5°C to 39.1°C). Uncommonly, the maintenance of homeothermy during moderate heat stress was achieved primarily by intense tachypnea (122mov/min). The sweating rate remained abnormally low under conditions of moderate heat stress, rising significantly (110gm−2h−1) without evidence of stabilization, only when tendency for heat storage occurred. This unusual response of the evaporative heat loss pathways infers a different thermoregulatory strategy, suggesting a different adaptation to semi-arid environment and strong association with water metabolism.

Lipopolysaccharide-induced fever alters Hering–Breuer reflex in anesthetized rats

The aim of the study was to test the hypothesis that control of breathing via Hering–Breuer reflex (HB) is influenced by lipopolysaccharide (LPS)-induced fever in rats. Animals were injected intraperitoneally with LPS and control group with an equivalent volume of saline. HB reflex was elicited by inflations of the lungs followed by occlusion of the airways under control of esophageal pressure. Duration of HB reflex (Tapnoe) was continuously reduced as body temperature rose during experiment. Compared to normothermic controls, animals with fever had significant shortening of Tapnoe at 240min and 300min after LPS administration. Fever was further accompanied by a reduction in the strength of HB reflex (inhibitory ratio, IR). In comparison with controls, significant decrease of IR was observed at 300min after LPS injection. Conclusion: altered neural control of breathing demonstrated by decreased power of Hering–Breuer inflation reflex in conditions of LPS-induced fever may facilitate thermal tachypnoea and/or play a role in the origin of respiratory instability accompanying febrile response.

Components and mechanisms of thermal hyperpnea

The pattern of breathing during a hyperthermia-induced hyperventilation varies across different species. Thermal tachypnea is a first phase panting response adopted during hyperthermia when tidal volume is minimized and the frequency of breathing is maximized. Blood-gas tensions and pH are maintained during this hyperventilation, and the associated heat loss helps the animal regulate its body temperature. A second pattern of breathing adopted in hyperthermia is thermal hyperpnea; this response is the focus of this review. This form of hyperventilation is evident after an increase in core temperature and it is apparent in humans. Increases of tidal volume as well as frequency of breathing are evident during this response that results in a respiratory alkalosis. The cause of thermal hyperpnea is not resolved; evidence of the potential mechanisms underlying this response support that modulators of the response act in either a multiplicative or additive manner with body temperatures. The details of the designs and methodologies of the studies supporting or refuting these two views are discussed. A physiological rationale for thermal hyperpnea is presented in which it is suggested this response serves a heat-loss role and contributes to selective brain cooling in hyperthermic humans. Ongoing research in this area is focused on resolving the mechanisms underlying thermal hyperpnea and its contribution to cranial thermoregulation. The direct application of this research is for the care of febrile and hyperthermic patients.

Dynamic Respiratory Responses to Preoptic/Anterior Hypothalamic Warming in the Sleeping Cat

Timing and amplitude characteristics of diaphragmatic muscle activity following bilateral local warming of the preoptic area/anterior hypothalamic region (POAH) were studied during sleep in free-moving, intact adult cats. Warming of the POAH increased local brain temperature by 1.4-3.7 degrees C and elicited thermal tachypnea (panting) during quiet sleep (QS). Following transition to rapid eye movement (REM) sleep, the tachypnea, initially induced by warming during QS, diminished, but respiratory rates remained above baseline REM levels, and an intermittent pattern of faster and slower breathing rates developed. In QS, tachypnea resulted primarily from a decline in inspiratory time (TI), whereas in REM sleep, reduction in expiratory time (TE) was more prominent. Although diaphragmatic electromyographic amplitude decreased by 40% during panting in QS, the much higher respiratory rates (+350%) resulted in apparent increases in relative ventilation and inspiratory drive. A less pronounced respiratory rate change (+46%) emerged during REM sleep, resulting in no significant changes in ventilation and inspiratory drive in response to warming in that state. The results suggest that descending thermal influences on respiratory patterning differ between QS and REM states in both overall respiratory rate and on relative TI and TE, and thus do not affect inspiratory drive exclusively.

Role of dopamine and arterial chemoreceptors in thermal tachypnea in conscious cats

In mammals submitted to a warm environment, intracerebral injection of dopamine (DA) produces no change or an increase in body temperature accompanied by an increase in metabolic heat production, but its effect on heat loss mechanisms such as vasodilation and tachypnea is not clear. Because the principal mechanism of heat loss in the conscious cat is thermal tachypnea, we studied the influence of DA on thermal tachypnea in response to heat stress (ambient temperature = 33-36 degrees C) in five conscious cats. We first studied the steady-state response to a DA agonist, apomorphine, which crosses the blood-brain barrier. Intravenous injection of apomorphine greatly reduced thermal tachypnea by decreasing respiratory frequency (from 94.9 to 52.5 breaths/min) and increasing tidal volume (from 13.2 to 20.4 ml). The subsequent injection of the DA antagonist haloperidol, which also crosses the blood-brain barrier, restored the initial tachypnea. To further investigate the mechanism involved in thermal tachypnea, we studied the influence of peripheral chemoreceptors by transiently stimulating or inhibiting carotid body (CB) activity during tachypneic breathing. CB stimulation by intravenous injection of NaCN or domperidone reduced thermal tachypnea mainly by decreasing the respiratory frequency, whereas CB inhibition by DA tended to increase frequency and thus tachypnea. It is concluded that 1) in a warm environment, central DA receptors are also greatly involved in heat loss mechanisms, 2) arterial chemoreceptor input appears to counteract this tachypneic breathing, and 3) thermal and hypoxic tachypnea may be controlled by the same mechanism in which a DA-like system has a key role.

Effect of upper airway CO2 on breathing in awake ponies.

We determined whether the [CO2] in the upper airways (UA) can influence breathing in ponies and whether UA [CO2] contributes to the attenuation of a thermal tachypnea during periods of elevated inspired CO2. Six ponies were studied 1 mo after chronic tracheostomies were created. For one protocol the ponies were breathing room air through a cuffed endotracheal tube. Another smaller tube was placed in the tracheostomy and directed up the airway. By use of this tube, a pump, and prepared gas mixtures, UA [CO2] was altered without affecting alveolar or arterial PCO2. When the ponies were at a neutral environmental temperature (TA) and breathing frequency (f) was 8 breaths X min-1, increasing UA [CO2] up to 18-20% had no effect on f. However, when TA was increased 20 degrees C to increase f to 50 breaths X min-1, then increasing UA [CO2] to 6% or to 18-20% reduced f by 5 +/- 1.7 (SE) and 12 +/- 1.6 breaths X min-1, respectively (t = 3.3, P less than 0.01). These data suggest that in the pony there exists a UA CO2-H+ sensory mechanism. For a second protocol the ponies were breathing a 6% CO2 gas mixture for 15 min in the normal fashion over the entire airway (nares breathing, NBr) or they were breathing this gas mixture for 15 min through the cuffed endotracheal tube (TBr). At a neutral TA, increasing inspired [CO2] to 6% resulted in a 6-breaths X min-1 increase in f during both NBr and TBr.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of hilar nerve denervation on breathing and arterial PCO2 during CO2 inhalation.

We determined the effects of denervating the hilar branches (HND) of the vagus nerves on breathing and arterial PCO2 (PaCO2) in awake ponies during eupnea and when inspired PCO2 (PICO2) was increased to 14, 28, and 42 Torr. In five carotid chemoreceptor-intact ponies, breathing frequency (f) was less, whereas tidal volume (VT), inspiratory time (TI), and ratio of TI to total cycle time (TT) were greater 2-4 wk after HND than before HND. HND per se did not significantly affect PaCO2 at any level of PICO2, and the minute ventilation (VE)-PaCO2 response curve was not significantly altered by HND. Finally, the attenuation of a thermal tachypnea by elevated PICO2 was not altered by HND. Accordingly, in carotid chemoreceptor-intact ponies, the only HND effect on breathing was the change in pattern classically observed with attenuated lung volume feedback. There was no evidence suggestive of a PCO2-H+ sensory mechanism influencing VE, f, VT, or PaCO2. In ponies that had the carotid chemoreceptors denervated (CBD) 3 yr earlier, HND also decreased f, increased VT, TI, and TT, but did not alter the slope of the VE-PaCO2 response curve. However, at all levels of elevated PICO2, the arterial hypercapnia that had persistently been attenuated, since CBD was restored to normal by HND. The data suggest that during CO2 inhalation in CBD ponies a hilar-innervated mechanism influences PaCO2 by reducing physiological dead space to increase alveolar ventilation.

Aspects of nasal heat exchange in resting reindeer.

Total respiratory heat loss (t.r.h.l.) in resting reindeer has been calculated from exhaled air temperature (Te) and respiratory minute volume (V) obtained during heat and cold stress in both summer and winter. Exhaled air temperature decreased with decreasing ambient temperature (Ta) in both summer and winter. The lowest Te recorded was +6 degrees C at a Ta of -45 degrees C in winter and the highest +38 degrees C at a Ta of + 29 degrees C in summer. At any Ta, Te was higher in winter than in summer. V was constant with increasing Ta up to +25 degrees C and -10 degrees C in summer and winter, respectively. Further increase in Ta resulted in thermal tachypnea. During summer t.r.h.l. did not change significantly in the ambient temperature range from -25 to +25 degrees C. In winter, however, t.r.h.l. increased linearly with increasing ambient temperature from -30 to +15 degrees C. Minimum t.r.h.l. was found to coincide with the animals' lower critical temperature. We suggest that the heat exchange in the upper respiratory tract of resting reindeer is actively regulated to attain fine tuning of thermal balance in this high arctic mammal undergoing great seasonal changes in fur insulation.

Blood gas changes during panting in a small East African antelope, the dik-dik.

Five adult male dik-dik (Madoqua kirkii) were exposed in a climatic chamber to an air temperature of 45 degrees C. Measurements were made of rectal temperature (Tre) and respiratory frequency (f) and arterial blood samples taken before and during heat exposure were analyzed for pH, PCO2 and PO2. During exposure, Tre and f increased in all animals. In the first 80 min dik-dik displayed thermal tachypnea and minor changes in blood gases. Continued exposure lead to hyperpnea accompanied by a fall in PaCO2 and a rise in pH. PaCO2 at first fell and then increased toward or above control levels. The dik-dik did not display second phase breathing. This observation confirms that second phase breathing is not essential to the development of respiratory alkalosis. The main conclusion of the study is that the dik-dik, unlike another heat-adapted antelope, the wildebeest (Taylor, Robertshaw, and Hoffmann. Am. J. Physiol. 217:907-910, 1969), is unable to resist alkalosis during heat stress.

Effect of thermal tachypnoea and of its mechanical or pharmacological inhibition on hypothalamic temperature in the sheep

The abrupt inhibition of breathing in the panting sheep, by mechanical blockage of the nostrils or by the injection of noradrenaline or carbachol into a lateral cerebral ventricle, causes an immediate rise in hypothalamic temperature, followed by a rise in that of the carotid artery blood. This confirms that evaporation from the surfaces of the upper respiratory tract has an immediate and local effect on brain temperature. The significance of this relation in a species which controls its core temperature particularly well is discussed.

Lingual blood flow and its hypothalamic control in the dog during panting.

1. The effects of increased ambient temperature (Ta) on blood-flow and -temperatures of the tongue were studied in the unanaesthetized dog. At Ta of 20 degrees C and a relative humidity (rh) of 30% the mean lingual blood flow was 11 ml-min-1 (0.15 ml-g-1-min-1) and the temperature difference between the lingual artery and vein (deltaTLAV) was 1.0 degrees C. Accordingly, a heat loss of 48.6 J-min-1 was calculated even for the dog breathing with the mouth closed. When Ta was elevated to 38 degrees C at constant rh, panting ensued. In parallel fashion lingual blood flow increased to 60.4 ml-min-1 (0.81 ml-g-1-min-1) in mean and to 74.7 ml-min-1 (0.99 ml-g-1-min-1) at peak rate of thermal tachypnoea (272 breaths-min-1). This flow increase resulted from a decrease in the local vascular resistance since the driving systemic pressure remained constant. It was accompanied by an increase in TLAV to 1.5 degrees C equivalent to a heat loss of 400.7J-min-1 in mean and 496.2J-min-1 at maximum respiratory rate. 2. The preoptic/anterior hypothalamic (PO/AH) region was heated with a water perfused thermode in urethane anaesthetized dogs at constant body temperature in order to study the relationship in time between the increase in lingual blood flow and the onset of thermal panting. Lingual blood flow was found to be 20 ml-min-1 at a respiratory rate of 60 breaths/min. During hypothalamic heating both respiratory rate and lingual blood flow increased markedly. At maximum respiratory rates (244 breaths-min-1) lingual blood flow reached a level of 60 ml-min-1. When perfusion of the thermode was stopped, both respiratory rate and lingual blood flow synchronously returned to control values within 5 min. Similar changes did not occur in dogs in which a ventilatory response failed to be elicited during hypothalamic heating. 3. The results suggest that the tongue contributes to the evaporative heat loss mechanism and they confirm the concept that panting, associated with increased lingual blood flow, is induced by a common autonomic outflow pattern which is mediated by the central mechanism controlling thermal homeostasis.

Inhibition of thermal tachypnoea in rabbits following exposure to cold and water deprivation.

1. Rabbits were clipped and exposed in turn to four environmental conditions: control (C), cold exposure (CE), water deprivation (WD) and water deprivation and cold exposure together (WD/CE). 2. Following each type of treatment, the rabbits were exposed for 1 hr to an ambient temperature (Ta) of 35 degrees C. During this time, respiratory frequency (RF), rectal temperature (Tre), activity and oxygen consumption (V02) were recorded. 3. It was found that under both cold exposure and water deprivation conditions, the mean respiratory frequency during the first 30 min of heat exposure was reduced when compared with controls. This was associated with a delay in the onset of thermal tachypnoea. Under conditions of water deprivation and cold exposure together, the mean respiratory frequency was further reduced and the length of the delay was increased. 4. Previous cold exposure led to an increase in the V02 measured at 35 degrees C, whereas the V02, after water deprivation and water deprivation and cold exposure together were not significantly different from the control. 5. Neither the initial Tre nor the change in the Tre during the course of the heat exposure were significantly different from the controls under any of the experimental conditions. 6. It is concluded that both water deprivation and previous cold exposure cause a block to panting in the heat and that the blocking mechanisms involved are closely interrelated. It is also concluded that neither the metabolic rate of the animal nor its initial or final Tre are important factors in determing the degree to which thermal tachypnoea is inhibited.

Climatic adaptation in recently shorn merino sheep.

Heart rates, respiratory rates, body temperatures, ad libitum ‘day’ and ‘night’ food consumption and body weight changes have been examined in 15 mature Merino wethers shorn in moderate environmental conditions. All sheep showed a depression in food consumption for two days after shearing. Sheep that gained weight during the next three weeks then increased their food consumption at night by approximately 30% although the average daily consumption was only increased by 5%. Sheep that lost weight showed a depressed food consumption throughout the three week period after shearing. Marked increases in the temperature difference between ear skin and air as well as thermal tachypnoea during the warmest period of the day were recorded in all sheep 14–16 days after shearing. This indicated that the critical temperature for all sheep had decreased by about 10°C. These signs of acclimatisation appeared at similar times in all sheep, suggesting that increased resistance to body cooling developed at similar rates in weight gain and weight loss sheep and independent of the origin of body heat production. The results of the investigations are discussed in relation to the concept that the initial response to cold stress includes a depression in food intake and that the duration of this depression is a function of the cold stimulus and the strain it induces in the sheep.

Delay in the onset of thermal tachypnoea in shorn sheep exposed to 42degrees C in winter and summer.

Shorn sheep were routinely exposed to ambient temperatures (Ta) of 14 and 42�C in a climatic chamber in winter and in summer. Rectal temperature (Tre) and skin temperature (Tsk) were measured at 14�C and the time elapsing between raising the Ta to 42�C and the onset of thermal tachypnoea was recorded. It was found that the onset of thermal tachypnoea in the heat was dependent upon the Ta to which the sheep had been previously exposed in the animal house and, in summer, the degree of fleece regrowth. There was an inverse linear relationship between the mean Tsk recorded immediately prior to raising the Ta and the delay in onset of thermal tachypnoea both in winter and summer. Thus, for either season, the inhibition of panting could be related to the degree of cold stimulation received from the periphery. However, a comparison of winter and summer data indicated that other factors were also involved. Tsk was significantly higher, and Tre significantly lower, in winter than in summer. These observations point towards possible seasonal changes in basal metabolic rate and thermoregulatory set-points. The results are discussed with regard to current theories concerning the mechanisms leading to the inhibition of thermal tachypnoea in shorn sheep.

Respiratory function during thermal tachypnoea in sheep.

1. Four Merino wethers were exposed to dry bulb temperatures ranging from approximately 20 to 60 degrees C, and the concurrent changes in respiratory frequency, tidal volume, respiratory minute volume, alveolar ventilation, dead space ventilation, carbon dioxide output, rectal temperature, and arterial and mixed venous blood, CO(2) content, CO(2) partial pressure and pH were established.2. The respiratory response to heat exposure showed two phases. Respiratory minute volume was initially increased by a rise in the respiratory frequency, while tidal volume decreased. After more prolonged exposure there was a second phase in which respiratory minute volume was further increased by an increase in the tidal volume; respiratory frequency was now slower than in the first phase but was still well above control values.3. The increase in respiratory minute volume during the first phase of the response was restricted almost entirely to the respiratory dead space; changes in blood CO(2) and pH were slight. In the second phase, respiratory minute volume showed a much greater increase, and a change of alveolar ventilation to about 5 times the control level resulted in severe respiratory alkalosis.4. Contrary to findings in cattle, the slower, deeper form of respiration could be elicited even with rectal temperature in the normal range. This change in respiration appears to be the result of either peripheral thermoreceptor function or mechanical demands of the respiratory system. The neglect of control of acid-base balance during the second phase indicates the existence of a dominant thermal stimulus or modification of respiratory control mechanisms.