Longitudinal distribution of canine respiratory heat and water exchanges

We assessed the longitudinal distribution of intra-airway heat and water exchanges and their effects on airway wall temperature by directly measuring respiratory fluctuations in airstream temperature and humidity, as well as airway wall temperature, at multiple sites along the airways of endotracheally intubated dogs. By comparing these axial thermal and water profiles, we have demonstrated that increasing minute ventilation of cold or warm dry air leads to 1) further penetration of unconditioned air into the lung, 2) a shift of the principal site of total respiratory heat loss from the trachea to the bronchi, and 3) alteration of the relative contributions of conductive and evaporative heat losses to local total (conductive plus evaporative) heat loss. These changes were not accurately reflected in global measurements of respiratory heat and water exchange made at the free end of the endotracheal tube. Raising the temperature of inspired dry air from frigid to near body temperature principally altered the mechanism of airway cooling but did not influence airway mucosal temperature substantially. When local heat loss was increased from both trachea and bronchi (by increasing minute ventilation), only the tracheal mucosal temperature fell appreciably (up to 4.0 degrees C), even though the rise in heat loss from the bronchi about doubled that in the trachea. Thus it appears that the bronchi are better able to resist changes in airway wall temperature than is the trachea. These data indicate that the sites, magnitudes, and mechanisms of respiratory heat loss vary appreciably with breathing pattern and inspired gas temperature and that these changes cannot be predicted from measurements made at the mouth. In addition, they demonstrate that local heat (and presumably, water) sources that replenish mucosal heat and water lost to the airstream are important in determining the degree of local airway cooling (and presumably, drying).     

Indirect assessment of mucosal surface temperatures in the airways: theory and tests

We developed and tested a method, based on conduction heat transfer analysis, to infer airway mucosal temperatures from airstream temperature-time profiles during breath-hold maneuvers. The method assumes that radial conduction of heat from the mucosal wall to inspired air dominates heat exchange during a breath-hold maneuver and uses a simplified conservation of energy analysis to extrapolate wall temperatures from air temperature vs. time profiles. Validation studies were performed by simultaneously measuring air and wall temperatures by use of a retractable basket probe in the upper airways of human volunteers and intrathoracic airways of paralyzed intubated dogs during breath holding. In both protocols, a good correlation was demonstrated between directly measured wall temperatures and those calculated from adjacent airstream temperature vs. time profiles during a breath hold. We then calculated intrathoracic bronchial wall temperatures from breath-hold airstream temperature-time profiles recorded in normal human subjects after cold air hyperpnea at 30 and 80 l/min. The calculations show airway wall temperatures in the upper intrathoracic airways that are below core body temperature during hyperpnea of frigid air and upper thoracic airways that are cooler than more peripheral airways. The data suggest that the magnitude of local intrathoracic heat/water flux is not represented by heat/water loss measurements at the airway opening. Both the magnitude and locus of heat transport during cold gas hyperventilation vary with changes in inspired gas temperature and minute ventilation; both may be important determinants of airway responses.     

Heat and water rate transfer processes in the human respiratory tract at various altitudes

The process of the respiratory air conditioning as a process of heat and mass exchange at the interface inspired air-airways surface was studied. Using a model of airways (Olson et al., 1970) where the segments of the respiratory tract are like cylinders with a fixed length and diameter, the corresponding heat transfer equations, in the paper are founded basic rate exchange parameters-convective heat transfer coefficient h(c)(W m(-2) degrees C(-1)) and evaporative heat transfer coefficient h(e)(W m(-2)hPa(-1)). The rate transfer parameters assumed as sources with known heat power are connected to airflow rate in different airways segments. Relationships expressing warming rate of inspired air due to convection, warming rate of inspired air due to evaporation, water diffused in the inspired air from the airways wall, i.e. a system of air conditioning parameters, was composed. The altitude dynamics of the relations is studied. Every rate conditioning parameter is an increasing function of altitude. The process of diffusion in the peripheral bronchial generations as a basic transfer process is analysed. The following phenomenon is in effect: the diffusion coefficient increases with altitude and causes a compensation of simultaneous decreasing of O(2)and CO(2)densities in atmospheric air. Due to this compensation, the diffusion in the peripheral generations with altitude is approximately constant. The elements of the human anatomy optimality as well as the established dynamics are discussed and assumed. The square form of the airways after the trachea expressed in terms of transfer supposes (in view of maximum contact surface), that a maximum heat and water exchange is achieved, i.e. high degree of air condition at fixed environmental parameters and respiration regime.     

Cold-induced changes in breathing pattern as a strategy to reduce respiratory heat loss

Thermoregulatory benefits of cold-induced changes in breathing pattern and mechanism(s) by which cold induces hypoventilation were investigated using male Holstein calves (1-3 mo old). Effects of ambient temperatures (Ta) between 4 and 18 degrees C on ventilatory parameters and respiratory heat loss (RHL) were determined in four calves. As Ta decreased, respiratory frequency decreased 29%, tidal volume increased 35%, total ventilation and RHL did not change, and the percentage of metabolic rate attributed to RHL decreased 26%. Total ventilation was stimulated by increasing inspired CO2 in six calves (Ta 4-6 degrees C), and a positive relationship existed between respiratory frequency and expired air temperature. Therefore, cold-exposed calves conserve respiratory heat by decreasing expired air temperature and dead space ventilation. Compared with thermoneutral exposure (16-18 degrees C), hypoventilation was induced by airway cold exposure (4-6 degrees C) alone and by exposing the body but not the airways to cold. Blocking nasal thermoreceptors with topical lidocaine during airway cold exposure prevented the ventilatory response but did not lower hypothalamic temperature. Hypothalamic cooling (Ta 16-18 degrees C) did not produce a ventilatory response. Thus, airway temperature but not hypothalamic temperature appears to control ventilation in cold-exposed calves.     

Interactions of respiration and the bradycardia of submersion in harbor seals.

Six harbor seals with percutaneous tracheostomies were artificially ventilated while immersed. Changes in the oxygen content of the inspired gas and in the minute-volume altered the magnitude of the bradycardia observed after the animal had been submerged for 30 s. The average heart rate in five seals changed from 16.7 (S.D. = 4.4) beats per minute during artificial ventilation with N2, to 58.7 (S.D. = 10.4) beats per minute while breathing air, but this cardiac chronotropic effect of oxygen was blocked by addition of 7% CO2 to the inspired gas. Ventilatory minute-volumes above approximately 3 litres/min caused cardiac acceleration in a manner related to ventilation; below this, changes in heart rate were inconsistent. While being artificially ventilated with air, the average heart rate in five seals changed from 16.5 beats per minute to 73.4 beats per minute as ventilation was increased from 0 to greater than 8 litres/min. These experiments demonstrate that O2, CO2, and ventilatory minute-volume have significant effects upon the heart rate of seals under water and suggest the presence of chemoreceptor-mediated effects on heart rate during submersion.     

Skinfolds and resting heat loss in cold air and water: temperature equivalence.

Fourteen male subjects with unweighted mean skinfolds (MSF) of 10.23 mm underwent several 3-h exposures to cold water and air of similar velocities in order to compare by indirect calorimetry the rate of heat loss in water and air. Measurements of heat loss (excluding the head) at each air temperature (Ta = 25, 20, 10 degrees C) and water temperature (Tw = 29-33 degrees C) were used in a linear approximation of overall heat transfer from body core (Tre) to air or water. We found the lower critical air and water temperatures to fall as a negative linear function of MSF. The slope of these lines was not significantly different in air and water with a mean of minus 0.237 degrees C/mm MSF. Overall heat conductance was 3.34 times greater in water. However, this value was not fixed but varied as an inverse curvilinear function of MSF. Thus, equivalent water-air temperatures also varied as a function of MSF. Between limits of 100-250% of resting heat loss the following relationships between MSF and equivalent water-air temperatures were found (see article).     

Mathematical modeling of heat and water transport in human respiratory tract

Excessive heat and water losses from the airways are stimuli to asthma. To study heat and water vapor transport in the human respiratory tract, a time-dependent model, based on a single differential equation with an analytical solution, was developed that could predict the intra-airway temperatures and water vapor contents. The key feature is the dependence of the temperature and water vapor along the respiratory tract as a function of the air residence time at each location. The model assumes disturbed laminar flow leading to enhanced transport mechanisms and wall temperature profiles modeled according to experimental data (E. R. McFadden, Jr., B. M. Pichurko, H. F. Bowman, E. Ingenito, S. Burns, N. Dowling, and J. Soloway. J. Appl. Physiol. 58: 564-570, 1985). It predicts that 1) the air equilibrates with the wall before it reaches body conditions (37 degrees C, 99.5% relative humidity); 2) conditioning of the inspired air involves several generations, with the number depending on the respiratory conditions; and 3) the walls of the upper airways are unsaturated, although it is difficult to judge at this state the depth of the respiratory tract affected.     

Respiratory heat loss in the sheep: a comprehensive model

A model is presented for the respiratory heat loss in sheep, considering both the sensible heat lost by convection ( C(R)) and the latent heat eliminated by evaporation ( E(R)). A practical method is described for the estimation of the tidal volume as a function of the respiratory rate. Equations for C(R) and E(R) are developed and the relative importance of both heat transfer mechanisms is discussed. At air temperatures up to 30 degrees C sheep have the least respiratory heat loss at air vapour pressures above 1.6 kPa. At an ambient temperature of 40 degrees C respiratory loss of sensible heat can be nil; for higher temperatures the transfer by convection is negative and thus heat is gained. Convection is a mechanism of minor importance for the respiratory heat transfer in sheep at environmental temperatures above 30 degrees C. These observations show the importance of respiratory latent heat loss for thermoregulation of sheep in hot climates.     

哺乳动物毛被传热性能及其影响因素

毛被能够加强或减弱动物向周围环境的热量散失,毛被的形态结构和颜色是传热性能的决定因素,其传热过程往往是传导、对流和辐射3个过程的耦合。以往研究发现环境因子中,风可增加机体向环境中的散热速率,且散失量与风速正相关,且动物通过调节在风场中的姿态来适应不同风向。动物体与环境间的温差是影响散热速率的另一因素,不同环境中的动物通过改变毛被结构来适应温差变化。毛被含水率上升会引起导热和蒸发冷却作用加强,动物通过行为或毛被结构变化来调节毛被含水率。毛色决定毛被吸收和反射热辐射的能力。毛被传热性能直接把动物的生理特点与环境因子关联起来,这对揭示动物的适应、进化都具有重要意义。同时提出,毛被结构和传热性能的研究还有助于仿生学意义的挖掘。因此,今后应重点在毛被结构和物理性能、研究技术与方法以及毛被生物学和仿生学意义等方面开展研究。     

Bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs

We demonstrated spontaneous self-limited bronchoconstriction after eucapnic dry gas hyperpnea in 22 anesthetized, mechanically ventilated guinea pigs pretreated with propranolol (1 mg/kg iv). Eucapnic hyperpnea "challenges" of room temperature dry or humidified gas (5% CO2-95% O2) were performed by mechanically ventilating animals (150 breaths/min, 3-6 ml tidal volume) for 5 min. During a "recovery" period after hyperpnea, animals were returned to standard ventilation conditions (6 ml/kg, 60 breaths/min, 50% O2 in air, fully saturated at room temperature). After dry gas hyperpnea (5 ml, 150 breaths/min), respiratory system resistance (Rrs) increased in the recovery period by 7.7-fold and dynamic compliance (Cdyn) decreased by 79.7%; changes were maximal at approximately 3 min posthyperpnea and spontaneously returned to base line in 10-40 min. This response was markedly attenuated by humidification of inspired air. Four consecutive identical dry air challenges resulted in similar posthyperpnea responses in four animals. Increasing the minute ventilation during hyperpnea (by varying tidal volume from 3 to 6 ml) caused increased bronchoconstriction in a dose-dependent fashion in six animals. Neither vagotomy nor atropine altered the airway response to dry gas hyperpnea. We conclude that dry gas hyperpnea in anesthetized guinea pigs results in a bronchoconstrictor response that shares five similar features with hyperpnea-induced bronchoconstriction in human asthma: 1) time course of onset and spontaneous resolution, 2) diminution with humidification of inspired gas, 3) reproducibility on consecutive identical challenges, 4) stimulus-response relationship with minute ventilation during hyperpnea, and 5) independence of parasympathetic neurotransmission.     

Thermal interaction between animal and microclimate: a comprehensive model

An equation based on heat transfer theory is developed to predict the rate of heat loss from a homeothermic vertebrate to the environment, specified by the air temperature, humidity, windspeed and radiation receipt. The analysis incorporates the animal's thermoregulatory responses--sweating ability, vasomotor action, and regulation of body-core temperature, metabolic and respiratory rate. The loss of heat and water vapour from cattle is used as an illustration, and particular attention is given to their heat balance in hot environments. The predicted rates of heat loss from cattle indoors at various air temperatures and humidities are consistent with experiments. Outdoors, intercepted solar radiation can reduce substantially heat loss through the body tissue when the air temperature is low. In contrast, at high air temperatures the heat dissipation may not be sensitive to the radiation load, although body-core temperature is. Increased rates of air movement can aggravate strain at low air temperatures, but mitigate strain in a hot environment.     

Sympathoadrenal response to repetitive exercise in normal and asthmatic subjects

To explore the role of catecholamine release in the pathogenesis of exercise-induced asthma, we had seven asthmatic and seven normal subjects undergo three hourly exercise challenges that were matched for inspired air temperature, minute ventilation, and relative work loads. Pulmonary mechanics and plasma epinephrine and norepinephrine were measured before, at end exercise, and serially after each challenge. There were no differences in the pattern of sympathoadrenal response of asthmatic and normal subjects, and both groups released sufficient quantities of epinephrine and norepinephrine into the peripheral circulation to allow these compounds to function as circulating hormones. As the catecholamines rose with repetitive exercise, progressive bronchodilation occurred in the asthmatics at the end of the work load, thus decreasing the apparent magnitude of the obstructive response. In addition to their effects on airway smooth muscle, the alpha-adrenergic actions of both catecholamines may have reduced airway wall hyperemia and edema. These data demonstrate that asthmatics do not have a defect in catecholamine release during exercise and that the physiological expression of exercise-induced asthma can be modulated by the sympathoadrenal epiphenomena that are associated with physical exertion.     

Alcohol and respiratory and body temperature changes during tepid water immersion

Resting subjects were immersed for 30 min in water at 22 and 30 degrees C after drinking alcohol. Total ventilation, end-tidal PCO2, rectal temperature, aural temperature, mean skin temperature, heart rate, and oxygen consumption were recorded during the experiments. Blood samples taken before the immersion period were analyzed by gas-liquid chromatography. The mean blood alcohol levels were 82.50 +/- 9.93 mg.(100 ml)-1 and 100.6 +/- 12.64 mg (100 ml)-1 for the immersions at 22 and 30 degrees C, respectively. There was no significant change in body temperature measured aurally or rectally, mean surface skin temperature, or heart rate at either water temperature tested. Total expired ventilation was significantly attenuated for the last 15 min of the immersion at 22 degrees C, after alcohol consumption as compared to the ventilation change in water at 22 degrees C without ethanol. This response was not consistently significantly altered during immersion in water at 30 degrees C. It is evident that during a 30-min immersion in tepid water with a high blood alcohol level, body heat loss is not affected but some changes in ventilation do occur.     

Reduction of the Pa(CO2) set point during hyperthermic exercise in the sheep

In animals that rely on the respiratory system for both gas exchange and heat loss, exercise can generate conflict between chemoregulation and thermoregulation. We hypothesized that in panting animals, hypocapnia during hyperthermic exercise reflects a reduction in the arterial CO2 tension (Pa(CO2)) set point. To test this hypothesis, five sheep were subjected to tracheal insufflations of CO2 or air (control) at 3-4 L min(-1) in 3 min bouts at 5 min intervals over 31 min of exercise. During exercise, rectal temperature and minute ventilation (V(E)) rose continuously while Pa(CO2) fell from 35.4+/-3.1 to 18.6+/-2.9 Torr and 34.3+/-2.4 to 18.7+/-1.5 Torr in air and CO2 trials, respectively. Air insufflations did not affect V(E) or Pa(CO2). V(E) increased during CO2 insufflations via a shift to higher tidal volume and lower frequency. CO2 insufflations also increased Pa(CO2), although not above the pre-exercise level. Within 5 min after each CO2 insufflation, Pa(CO2) had decreased to match that following the equivalent air insufflation. These results are consistent with a reduced Pa(CO2) set point or an increased gain of the Pa(CO2) regulatory system during hyperthermic exercise. Either change in the control of Pa(CO2) could facilitate respiratory evaporative heat loss by mitigating homeostatic conflict.     

Computation of respiratory heat exchanges

Two sets of equations have been proposed to estimate the convective or sensible (WCV) and the evaporative or insensible (WEV) respiratory heat exchanges. They are applicable both at sea-level barometric pressure with air breathing (SLA) and in hypo- or hyperbaria in both air (HA) and artificial (HAA) atmospheres. The only environmental parameters required are in SLA: the temperature (TI) and the partial pressure of water vapor of the inspired air (PIH2O); in HA: TI, PIH2O, and the actual barometric pressure (PB); and in HAA: IT, PIH2O, PB, the volumetric mass (rho mix), and the specific heat (cp mix) of the breathed gas mixture. When no physiological data are available the results are expressed in energy units per liter of pulmonary ventilation (WCV/V and WEV/V) in J X dm-3 BTPS. If the ventilation value (V) is known the results are obtained in units of power (W).     

Effect of CO₂ on the ventilatory sensitivity to rising body temperature during exercise

We examined the degree to which ventilatory sensitivity to rising body temperature (the slope of the regression line relating ventilation and body temperature) is altered by restoration of arterial PCO(2) to the eucapnic level during prolonged exercise in the heat. Thirteen subjects exercised for ~60 min on a cycle ergometer at 50% of peak O(2) uptake with and without inhalation of CO(2)-enriched air. Subjects began breathing CO(2)-enriched air at the point that end-tidal Pco(2) started to decline. Esophageal temperature (T(es)), minute ventilation (V(E)), tidal volume (V(T)), respiratory frequency (f(R)), respiratory gases, middle cerebral artery blood velocity, and arterial blood pressure were recorded continuously. When V(E), V(T), f(R), and ventilatory equivalents for O(2) uptake (V(E)/VO(2)) and CO(2) output (V(E)/VCO(2)) were plotted against changes in T(es) from the start of the CO(2)-enriched air inhalation (ΔT(es)), the slopes of the regression lines relating V(E), V(T), V(E)/VO(2), and V(E)/VCO(2) to ΔT(es) (ventilatory sensitivity to rising body temperature) were significantly greater when subjects breathed CO(2)-enriched air than when they breathed room air (V(E): 19.8 ± 10.3 vs. 8.9 ± 6.7 l·min(-1)·°C(-1), V(T): 18 ± 120 vs. -81 ± 92 ml/°C; V(E)/VO(2): 7.4 ± 5.5 vs. 2.6 ± 2.3 units/°C, and V(E)/VCO(2): 7.6 ± 6.6 vs. 3.4 ± 2.8 units/°C). The increase in Ve was accompanied by increases in V(T) and f(R). These results suggest that restoration of arterial PCO(2) to nearly eucapnic levels increases ventilatory sensitivity to rising body temperature by around threefold.     

Effects of atropine on respiratory heat loss in asthma

We have previously observed that although atropine does not alter the magnitude of the response to exercise while breathing cold air, it does cause the predominant site of obstruction to move into the lung periphery. To determine if this effect was due to changes in the conditioning of inspired air, we measured respiratory heat loss (RHL) and retrotracheal (Trt) and retrocardiac esophageal temperature in eight asthmatics while they performed eucapnic hyperventilation with cold air before and after the inhalation of atropine. Multiple aspects of pulmonary mechanics were also recorded. Significant and equivalent airway obstruction developed with and without atropine (control delta FEV1 = 1.0 +/- 0.2 (SE) liter; postatropine = 0.9 +/- 0.3 liter). Despite this, RHL was 17.1% greater and Trt fell 16% more after atropine. These data demonstrate that atropine can influence heat transfer within the lung and alter the sites of conditioning.     

Ventilatory response to sustained hypoxia in normal adults

We examined the ventilatory response to moderate (arterial O2 saturation 80%), sustained, isocapnic hypoxia in 20 young adults. During 25 min of hypoxia, inspiratory minute ventilation (VI) showed an initial brisk increase but then declined to a level intermediate between the initial increase and resting room air VI. The intermediate level of VI was a plateau that did not change significantly when hypoxia was extended up to 1 h. The relation between the amount of initial increase and subsequent decrease in ventilation during constant hypoxia was not random; the magnitude of the eventual decline correlated confidently with the degree of initial hyperventilation. Evaluation of breathing pattern revealed that during constant hypoxia there was little alteration in respiratory timing and that the changes in VI were related to significant alterations in tidal volume and mean inspiratory flow (VT/TI). None of the changes was reproduced during a sham control protocol, in which room air was substituted for the period of low fractional concentration of inspired O2. We conclude that ventilatory response to hypoxia in adults is not sustained; it exhibits some biphasic features similar to the neonatal hypoxic response.     

Effect of cold air inhalation on core temperature in exercising subjects under heat stress

Whether increasing respiratory heat loss (RHL) during exercise under heat stress can contain elevation of rectal temperature (Tre) was examined. Eight men cycled twice at 45-50% their maximum work rate until exhaustion at ambient temperature and relative humidity of 38 degrees C and 90-95%, respectively. They inspired either cold (3.6 degrees C) or ambient air in random sequence. When subjects breathed cold air during 23 min of exercise, a ninefold increase in RHL was observed vs. similar work during hot air inhalation (32.81 vs. 3.46 W). Respiratory frequency (f) and rate of rise in Tre decreased significantly (P less than or equal to 0.004 and P less than or equal to 0.002, respectively). The rise in skin temperature in each inhalant gas condition was accompanied by a parallel almost equal increase in core temperature above basal (delta Tre) for equivalent gains in skin temperature. The increase in tidal volume and decreased f in the cold condition allowed more effective physical conditioning of cold inspirate gas in the upper airways and aided RHL. Cold air inhalation also produced a significant (P less than or equal to 0.05) decrease in heart rate vs. hot air inhalation in the final stages of exercise. Insignificant changes in O2 consumption and total body fluid loss were found. These data show that cold air inhalation during exercise diminishes elevation of Tre and suggest that both the intensity and duration of work can thus be extended. The importance of the physical exchange of heat energy and any physiological mechanisms induced by the cold inspirate in producing the changes is undetermined.     

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.