Kybernetische Aspekte der Wärmetachypnoe

Summary The panting mechanism is considered as resulting from the joint effort of the two systems regulating the body temperature and the blood gas tensions respectively. Equations are derived which describe the equilibrium conditions for each system. A nomogram for the evaluation of the amount of heat taken up by one liter of respiratory air is given. Combination of the equilibrium equations leads to a infinite series due to the fact that heat dissipation by the respiratory tract involves increased heat production by the respiratory muscles. The conditions of convergence for the infinite series are derived assuming a quadratic relation between heat production of the respiratory muscles and respiratory minute volume. It is shown that the system will become unstable if the series diverges. Equations for the partial washout of the dead space are given which are essential for the independent control of alveolar ventilation and dead space ventilation by proper adjustment of tidal volume and respiratory rate. Two examples demonstrate the limited value of the panting mechanism as compared with the heat dissipation by sweat production, when the animals are subjected to high environmental temperatures. Panting seems superior however for eliminating an increased heat production due to muscular exercise at very low temperatures as for instance in sled dogs.     

Pulmonary gas exchange in panting dogs

Pulmonary gas exchange during panting was studied in seven conscious dogs (32 kg mean body wt) provided with a chronic tracheostomy and an exteriorized carotid artery loop. The animals were acutely exposed to moderately elevated ambient temperature (27.5 degrees C, 65% relative humidity) for 2 h. O2 and CO2 in the tracheostomy tube were continuously monitored by mass spectrometry using a special sample-hold phase-locked sampling technique. PO2 and PCO2 were determined in blood samples obtained from the carotid artery. During the exposure to heat, central body temperature remained unchanged (38.6 +/- 0.6 degrees C) while all animals rapidly switched to steady shallow panting at frequencies close to the resonant frequency of the respiratory system. During panting, the following values were measured (means +/- SD): breathing frequency, 313 +/- 19 breaths/min; tidal volume, 167 +/- 21 ml; total ventilation, 52 +/- 9 l/min; effective alveolar ventilation, 5.5 +/- 1.3 l/min; PaO2, 106.2 +/- 5.9 Torr; PaCO2, 27.2 +/- 3.9 Torr; end-tidal-arterial PO2 difference [(PE' - Pa)O2], 26.0 +/- 5.3 Torr; and arterial-end-tidal PCO2 difference, [(Pa - PE')CO2], 14.9 +/- 2.5 Torr. On the basis of the classical ideal alveolar air approach, parallel dead-space ventilation accounted for 54% of alveolar ventilation and 66% of the (PE' - Pa)O2 difference. But the steepness of the CO2 and O2 expirogram plotted against expired volume suggested a contribution of series in homogeneity due to incomplete gas mixing.     

Ventilatory accommodation of oxygen demand and respiratory water loss in kangaroos from mesic and arid environments, the eastern grey kangaroo (Macropus giganteus) and the red kangaroo (Macropus rufus)

We studied ventilation in kangaroos from mesic and arid environments, the eastern grey kangaroo (Macropus giganteus) and the red kangaroo (Macropus rufus), respectively, within the range of ambient temperatures (T(a)) from -5 degrees to 45 degrees C. At thermoneutral temperatures (Ta=25 degrees C), there were no differences between the species in respiratory frequency, tidal volume, total ventilation, or oxygen extraction. The ventilatory patterns of the kangaroos were markedly different from those predicted from the allometric equation derived for placentals. The kangaroos had low respiratory frequencies and higher tidal volumes, even when adjustment was made for their lower basal metabolism. At Ta>25 degrees C, ventilation was increased in the kangaroos to facilitate respiratory water loss, with percent oxygen extraction being markedly lowered. Ventilation was via the nares; the mouth was closed. Differences in ventilation between the two species occurred at higher temperatures, and at 45 degrees C were associated with differences in respiratory evaporative heat loss, with that of M. giganteus being higher. Panting in kangaroos occurred as a graded increase in respiratory frequency, during which tidal volume was lowered. When panting, the desert red kangaroo had larger tidal volumes and lower respiratory frequencies at equivalent T(a) than the eastern grey kangaroo, which generally inhabits mesic forests. The inference made from this pattern is that the red kangaroo has the potential to increase respiratory evaporative heat loss to a greater level.     

Ventilation and acid-base balance in awake dogs exposed to heat and CO2

Some awake quiet dogs pant at cool ambient temperature (Ta) and some do not pant even when acutely exposed to heat. The purpose of the study was to determine whether this puzzling variability in respiratory behavior diminished during prolonged heat. The contributions of thermal and CO2 drives to respiratory adaptations were also examined. Five awake dogs acclimated to 20 degrees C were studied before and 2 and 48 h following exposure to 30-31 degrees C. Rectal temperature did not change; the important thermal stimulus, even at 48 h, appeared to be the increase in peripheral temperature. Variability between nonpanting and panting persisted over 48 h. On the average, ventilation (VE) doubled during heat, largely due to increased dead space ventilation. Nonpanting dogs at cool Ta decreased the threshold of the ventilatory response to CO2. A panting dog at cool Ta changed its slope of the ventilatory response from negative to positive. During hypercapnia in acute heat, ventilatory pattern changed so that frequency increased and tidal volume decreased for a given VE. By 48 h of heat, the ventilatory response to CO2 returned to control in only two dogs, but the ventilatory pattern during hypercapnia returned to control in four dogs. Since thermal stimuli remained unchanged at 48 h, adaptations of respiratory control may have been related to progressive adjustments of strong ions and acid-base balance.     

Control of panting in the desert iguana: roles for peripheral temperatures and the effect of dehydration

Although it is generally held that panting is a physiological mechanism for the regulation of brain temperature during heat stress, a number of studies have pointed to the importance of peripheral input for the initiation of the panting response in a variety of animals. By presenting ambient heat loads of 47 degrees, 54 degrees, 58 degrees, and 65 degrees C, and measuring skin, ear and core temperatures of the desert iguana, Dipsosaurus dorsalis, at the onset of panting, we found that the skin temperature at panting onset was independent of ambient heat load. This suggests that skin (peripheral) temperature is the body temperature on which the central thermoregulatory center cues to initiate thermal panting. Peripheral temperature control of panting was retained when the plasma osmolality of the desert iguana was increased by 100 mOsm/kg H2O to simulate dehydration. Dehydration to 80% initial body weight (IBW) resulted in a progressive increase in panting threshold (skin) from 42 degrees C for untreated lizards to 42.5 degrees C at 90% IBW to 43.3 degrees C at 80% IBW. Injection of 80% IBW lizards with a volume of 10 mM NaCl equivalent to weight loss resulted in a decrease in panting threshold to 40.8 degrees C. Injection with 1% body weight 3000 mM NaCl produced a dramatic increase in panting threshold to 45.9 degrees C. These data suggest that the desert iguana responds to dehydration by elevating panting threshold, thus promoting water conservation. These data also suggest that changes in plasma osmolality may be involved in the "setting" of panting threshold.     

Panting in reindeer (Rangifer tarandus)

Two winter-insulated Norwegian reindeer (Rangifer tarandus tarandus) were exposed to air temperatures of 10, 20, 30, and 38 degrees C while standing at rest in a climatic chamber. The direction of airflow through nose and mouth, and the total and the nasal minute volumes, respectively, were determined during both closed- and open-mouth panting. The animals alternated between closed- and open-mouth panting, but the proportion of open-mouth panting increased with increasing heat load. The shifts from closed- to open-mouth panting were abrupt and always associated with a rise in respiratory frequency and respiratory minute volume. During open-mouth panting, the direction of airflow was bidirectional in both nose and mouth, but only 2.4 +/- (SD) 1.1% of the air was routed through the nose. Estimates suggest that the potential for selective brain cooling is markedly reduced during open-mouth panting in reindeer as a consequence of this airflow pattern.     

Panting and acid-base regulation in heat stressed birds

1. Studies in respiratory physiology and acid-base balance of panting birds exposed to high Tas show that flying as well as nonflying birds can use the respiratory system simultaneously for gas exchange and evaporative cooling. 2. The present study proves that well acclimated hand-reared birds can effectively regulate a normal CO2 level and acid-base status in arterial blood, when exposed to extremely high temperatures (50-60 degrees C). 3. In many birds practising simple or "flush-out" panting, the dead space can be reduced to a volume which is estimated to be approx 15% the volume of the respiratory tract. 4. These two modes of ventilation, shallow and high-rate, restricted to the nonrespiratory surfaces, may ensure the avoidance of CO2-washout and limit lung ventilation to the volumes needed for oxygen consumption. 5. This view supports earlier theories, suggesting the existence of physiological shunt mechanisms which operate during thermal panting in birds.     

CNS thermosensitivity and control of latent heat dissipation in the pigeon

Thermoregulatory responses to heat exposure were studied in 12 hand-reared, acclimated pigeons (Columbia livia). Measurements of body temperature (Tcl), brain temperature (Tbr), cutaneous water evaporation (CWE) and respiratory frequency (fr) were carried out in intact conscious heat exposed birds. In a second group of lightly restrained birds, fr and CWE were taken when temperatures of the trunk, brain and air (Ta) were independently changed. Increasing Tbr to 43.5–43.8°C induced a pronounced polypnea (deep and fast, (300 breaths min⁻¹) when Tcl regulated at 42.4°C. Moreover, when hyperthermia (Tcl = 43.0°C) was combined with increased Tbr (43.0–43.8°C) shallow and fast panting (>500 breaths min⁻¹) was evoked. CWE was probably elicited by inputs generated by the skin warm receptors as a result of increased Ta. Moreover it was demonstrated that warming the brain to 42.5°C elicits cutaneous water evaporation in birds exposed to 26°C. When a high Ta (60°C) is accompanied by a high relative humidity (17%), the combined effect generates inputs eliciting intensive panting. The integration of the present and earlier data allows us to generate a model demonstrating the distinguished significance of the trunk, skin and brain thermosensors in the regulation of both respiratory and cutaneous latent heat dissipation. The present model also emphasizes the fact that the highly thermosensitive pigeon brain responds in a similar pattern to that found in mammals     

Respiratory evaporation in panting fowl: Partition between the respiratory and buccopharyngeal pumps

Summary Ventilation (V) and respiratory water loss were measured in domestic fowlGallus gallus subjected to raised environmental temperatures (33±2°C) and breathing air, 8% O₂ in N₂, 3% CO₂ in air or 5% CO₂ in air. Birds breathing air underwent an 18.6-fold increase in respiratory frequency and a 5-fold reduction in tidal volume and panting was accompanied by vigorous gular flutter. Hypoxic and hypercapnic birds breathed more slowly and deeply and gular flutter was strongly inhibited. The ratio was similar to that predicted on the basis of the measured ventilation assuming saturation of expired gas at measured gular mucosal temperature in hypoxic and hypercapnic birds but 54% greater than the predicted value in birds panting in air. It is concluded that the excess water loss during normal panting results from tidal airflow generated independently by the buccopharyngeal pump and that buccopharyngeal ventilation is equivalent to 54% of the respiratory ventilation.     

Ventilatory accommodation of oxygen demand and respiratory water loss in a large bird,the emu (Dromaius novaehollandiae), and a re-examination of ventilatory allometry for birds

Ventilation was studied in the emu, a large flightless bird of mass 40kg, within the range of ambient temperatures from-5 to 45°C. Data for the emu and 21 other species were used to calculate allometric relationships for resting ventilatory parameters in birds (breath frequency=13.5 mass^-0.314; tidal volume=20.7 mass^1.0). At low ambient temperatures the ventilatory system must accommodate the increased metabolic demand for oxygen. In the emu this was achieved by a combination of increased tidal volume and increased oxygen extraction. Data from emus sitting and standing at-5°C, when metabolism is 1.5x and 2.6x basal metabolic rate, respectively, indicate that at least in the emu an increase in oxygen extraction can be stimulated by low temperature independent of oxygen demand. At higher ambient temperatures ventilation was increased to facilitate respiratory water loss. The emu achieved this by increased respiratory frequency. At moderate heat loads (30–35°C) tidal volume fell. This is usually interpreted as a mechanism whereby respiratory water loss can be increased without increasing parabronchial ventilation. At 45°C tidal volume increased; however, past studies have shown that CO₂ washout is minimal under these conditions. The mechanism whereby this is possible is discussed.Abbreviations BMR basal metabolic rate - BTPS body temperature, ambient pressure, saturated - EO ₂ oxygen extraction - EWL evaporative water loss - f _R ventilation frequency - RH relative humidity - RHL respiratory heat loss - SEM standard error of the mean - SNK student-Newman-Keuls multiple range test - STPD standard temperature and pressure, dry - T _a ambient temperatures(s) - T _b body temperature(s) - T _ex expired air temperature(s) - T _rh chamber excurrent air temperature - V _J ventilation - VO₂ oxygen consumption - V _T tidal volume - V/Q air ventilation to blood perfusion ratio     

Sample-hold technique for analysis of respiratory gas composition at high breathing frequencies

A gas sampling device is described for continuous monitoring of respiratory gas composition that is applicable to experimental conditions when the breathing frequency is very high (greater than 2 Hz) and the response time of conventional gas analyzers becomes a critical limiting factor. The system utilizes the principle of discontinuous gas collection at any selected point of the respiratory cycle facilitated by ultraspeed piezoelectric valves and includes provision for sample-hold characteristics. Two distinct modes of operation are supported. In phase-locked mode gas sampling is synchronous with breathing frequency. In scanning mode gas collection is asynchronous with breathing frequency. Phase-locked mode may be used for continuous monitoring of end-tidal gas concentrations, whereas scanning mode is intended for assessing the gas concentration profile throughout the respiratory cycle. The system may be applied to steady breathing encountered in mechanical ventilation at high frequency or during quasi-steady breathing observed in panting animals. Combined with a respiratory mass spectrometer, the system has been used for measurement of gas concentrations in alveolar gas mixtures at breathing frequencies ranging from 3 to 30 Hz that were otherwise not amenable to rapid measuring techniques.     

Interaction of hypoxic and hypercapnic stimuli on breathing pattern in the newborn rat

We aimed to investigate whether newborn rats respond to acute hypoxia with a biphasic pattern as other newborn species, the characteristics of their ventilatory response to hypercapnia, and the ventilatory response to combined hypoxic and hypercapnic stimuli. First, we established that newborn unanesthetized rats (2-4 days old) exposed to 10% O2 respond as other species. Their ventilation (VE), measured by flow plethysmography, immediately increased by 30%, then dropped and remained around normoxic values within 5 min. The drop was due to a decrease in tidal volume, while frequency remained elevated. Hence, alveolar ventilation was about 10% below normoxic value. At the same time O2 consumption, measured manometrically, dropped (-23%), possibly indicating a mechanism to protect vital organs. Ten percent CO2 in O2 breathing determined a substantial increase in VE (+47%), indicating that the respiratory pump is capable of a marked sustained hyperventilation. When CO2 was added to the hypoxic mixture, VE increased by about 85%, significantly more than without the concurrent hypoxic stimulus. Thus, even during the drop in VE of the biphasic response to hypoxia, the respiratory control system can respond with excitation to a further increase in chemical drive. Analysis of the breathing patterns suggests that in the newborn rat in hypoxia the inspiratory drive is decreased but the inspiratory on-switch mechanism is stimulated, hypercapnia increases ventilation mainly through an increase in respiratory drive, and moderate asphyxia induces the most powerful ventilatory response by combining the stimulatory action of hypercapnia and hypoxia.     

Ventilatory and cardiovascular responses of the unanaesthetized chicken, Gallus domesticus, to the respiratory stimulants etamiphylline and almitrine

The ventilatory and cardiovascular effects of i.v. administration of the respiratory stimulants etamiphylline and almitrine were investigated in conscious or decerebrate adult female domestic fowl. Infusion of etamiphylline (100 mg . kg-1) or injection of almitrine (2 mg . kg-1) evoked a potent long-lasting stimulation of ventilation in both conscious and decerebrate fowl. The pattern of the respiratory response was characteristically different to that observed in mammals in that the increased minute volume of ventilation was attained by large increases in respiratory frequency accompanied by a reduction in tidal volume. The pattern of respiration following drug-induced stimulation was, in some birds, typical of thermal panting although neither etamiphylline nor almitrine caused significant increases in body temperature. Differences in the pattern of responses of the rate and depth of breathing may be attributed in part to the differences in pulmonary receptor systems involved in the control of breathing in birds and mammals.     

The redistribution of cardiac output in the dog during heat stress

In conscious Greyhound dogs, radioactive microsphere techniques have been used to measure cardiac output, its regional distribution, and proportion of the cardiac output passing through arteriovenous anastomoses (AVA's) in a thermoneutral environment and during severe heat stress. Heat stress resulted in a 74% increase in cardiac output and 4–6% of the cardiac output passed through AVA's. compared with about 1% under thermoneutral conditions: blood flow rate increased in skin of the lower legs and ears, tongue, maxillo turbinals, nasal mucosa, respiratory muscles and spleen, decreased in the thyroids, brain and spinal cord, and did not change significantly in the non-respiratory muscles, heart, pituitary, adrenals, kidneys, liver, stomach and intestines. Thus the circulatory requirements of the heat stressed dogs were met partly by an increase in cardiac output and partly by changes in its distribution. In contrast, the Merino sheep meets such a situation entirely by a redistribution of cardiac output. The present results may be taken as evidence that the Greyhound dog is less heat tolerant than the Merino sheep. The decreased brain blood flow during heat stress is similar to that which occurs in the sheep, but contrast with previous results obtained on anaestherized dogs. The less marked redistribution of cardiac output in the dog compared with the sheep, may explain the apparent difference in energy cost of panting in the two species.     

Depression of ventilation hypoxia in man.

In five normal male subjects, ventilation, PaO2, and PaCO2 were measured during the rapid progressive isocapnic production of hypoxia (5 min) and during the equally rapid isocapnic reversal of hypoxia. At similar PaO2, PaCO2, and pH, ventilation was less at a time when alveolar PO2 was increasing than when alveolar PO2 was decreasing. We interpret these results as showing that human ventilation is depressed by mild-to-moderate hypoxia (40-60 Torr), that such depression is probably central, and that it is ordinarily masked by peripheral chemoreceptor stimulation. We are not able to distinguish whether the ventilatory depression is caused by decreased central chemoreceptor PCO2 due to an increase in cerebral flow, direct hypoxic depressing of the central respiratory mechanism, or both.     

Relationship between hypercapnic and hypoxic stimuli of respiration during muscular activity]

Pulmonary ventilation (V) and alveolar gas composition (PACO2, PAO2) were studied in 12 healthy men who performed gradual muscular work under conditions of controlled hypercapnia, hypoxia, hyperoxia or their combinations. The respiratory response was estimated by absolute values of ventilation at the given PACO2 value and by its rise by 1 mm Hg of increased PACO2 (delta V/delta PACO2) under rest and under transitional and steady-state exercise. The exercise on-switch was accompanied by displacement to the top and an increased slope of the response curve (delta V/delta PACO2) not related to the work load. These changes suggest multiplicative interaction of the neurogenic and hypercapnic drives in the load switch-on. During steady-state exercise an important role of the hypoxic drive was revealed: hypoxemia induced a shift of the delta V/delta PACO2 response curve to a higher level, especially with the great work load. Thus the positive interaction between the hypercapnic and hypoxic respiratory drive augments with muscular exercise.     

Metabolism and evaporative heat loss in the dik-dik antelope (Rhynchotragus kirki)

1. Under controlled conditions, the rate of oxygen consumption (VO2) respiratory frequency, evaporative water loss, heat balance, rectal (Trec) and surface temperatures were determined in the dik-dik antelopes at ambient temperatures (Ta) ranging from 1 to 44 degrees C. 2. The thermal neutral zone was found to be between 24 and 35 degrees C. 3. Respiratory frequency ranged between 27 and 630 breaths/min. 4. At a Ta of 44 degrees C, 95% of the heat produced by the dik-dik was lost via respiratory evaporation. Despite an increase in Trec, cutaneous evaporation did not increase. 5. During panting, VO2 increased in accordance with the expected Q10 effect, contrary to earlier findings. 6. Measurements of circadian rhythm [LD 12:12 (7-19) CT26 degrees C] in VO2 showed that the minimum VO2 (0.42 ml O2/g/hr) occurred at midnight while the maximum (0.78 ml O2/g/hr) occurred at midday. The 24 hr mean VO2 was 0.61 ml O2/g/hr. 7. These measurements suggest that in nature, determinants other than light may be responsible for triggering the variations observed in VO2.     

Evaporative losses of water by birds

1. Birds lose water in evaporation from the respiratory tract and, in many species, through the skin. Anatomical arrangements in the nasal passages to conservation of water and hear from the expired air in the absence of heat loads. However, most species still expend more water in evaporation than they produce in metabolism when either quiescent or vigorously active. Certain small birds, several of them associated with arid environments, represent exceptions to this and their more favorable situation appears in part to reflect as an ability to curtail cutaneous water loss. 2. Birds typically resort to panting in dealing with substantial heat loads developing in hot environments or accumulated over bouts of activity. In a number of species this form of evaporative cooling is supplemented by gular fluttering. 3. The ubiquitousness of active heat defense appears to reflect more the importance for birds of dealing with heat loads existing following flight or sustained running than any universal affinity for hot climates. Panting can be sustained for hours, despite progressive dehydration and, in some instances, hypocapnia and respiratory alkalosis. The prominent involvement of thermoreceptors in the spinal cord in its initiation is of considerable interest.     

Physiological Responses Of Birds To Flight And Running

1. The energy required for sustained physical activity in flying and running birds is obtained from fatty acids mobilized from adipose stores under the influence of hormones. There is some evidence that glucagon, insulin and growth hormone may be involved in this process. 2. Energy expenditure can increase up to 14 times and 12 times resting values in flying and running birds, respectively. Energy expenditure varies only slightly over the normal range of flight speeds in individual species, but in running birds there is a linear correlation between oxygen consumption and speed. The slope of this relationship is an inverse function of body weight and indicates the energy cost of transport in ml O₂.kg^-1.m^-1. 3. Increased oxygen demands by the working muscles are met by increased ventilation and circulation. Increased oxygen delivery by the blood is achieved by rises in cardiac output and oxygen extraction. Cardiac stroke volume changes relatively little and the increased cardiac output results mainly from an increase in heart rate. Regional blood distribution during exercise may be determined not only by the demands of the locomotory muscles but also by the need to increase heat loss from the skin and respiratory tract. 4. Ventilatory movements during flight are frequently synchronized in a I:I fashion with wing movements. Increased ventilation during flight and running may be stimulated, not only by the need for increased gas exchange, but also in order to raise heat loss by respiratory evaporation. Thermal hyperventilation carries a risk of CO, washout from the lungs and consequent blood alkalosis. The risk is minimized in some species by appropriate alterations in the rate and depth of breathing, which help to confine excess ventilation to the respiratory dead space. 5. Metabolic heat produced during exercise is either lost from the respiratory linings and the skin, or stored by the body with a resultant rise in body temperature. Changes in peripheral blood perfusion and active regulation of the feathers may assist cutaneous heat loss. Respiratory evaporation usually accounts for less than 30% of the total heat loss, even at high air temperatures, and becomes progressively less efficient at higher exercise intensities. At high air temperatures and high exercise intensities, most of the metabolic heat is stored, and exercise duration is limited as the body temperature approaches the upper lethal limit.     

Differential responses of the airways and pulmonary tissues to inhaled histamine in young dogs

Airway and pulmonary tissue responses to aerosolized histamine were studied in five mongrel puppies (8-10 wk old). Alveolar pressure was measured by use of alveolar capsules and respiratory mechanics calculated during tidal ventilation and flow interruptions. Aerosolized histamine caused an increase in the tissue viscoelastic properties, which was measured as an increase in pulmonary resistance during tidal ventilation. An increase in stress recovery of the pulmonary tissues was measured with the interrupter technique after aerosolized histamine. These data demonstrate that aerosolized histamine caused an increase in the tissue viscoelastic properties. The most reasonable explanation for the mechanism of this increase would seem to be via reflex pathways stimulated by centrally located receptors.