Effect of hypercapnia on thermoregulation at high ambient temperature

The reported investigations were carried out on rabbits exposed for three hours to ambient temperature of 25 degrees C or 35 degrees breathing athmospheric air (controls) or gas mixtures containing 4% or 7% of CO2. During the exposure to 35 degrees C in rabbits breathing the gas mixture with 7% of CO2 the rise of rectal temperature was significantly greater, heat elimination from the auricular surface was increased, whereas the oxygen uptake was increased insignificantly. In tracheostomized rabbits breathing the gas mixture with 7% of CO2 at 32 degrees C the respiratory rate decreased but the respiration volume increased as compared with the animals breathing atmospheric air. It seems that the hyperthermic effect of hypercapnia demonstrated in this work can be attributed to the impairment of heat elimination through the upper airways due to an inhibition of thermal panting.     

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).     

Temperature regulation in adult quail (Colinus virginianus) during acute thermal stress

1. Evaporative heat loss, O2 consumption, CO2 production, and internal body temperature were measured in unanesthetized, unrestrained bobwhite (Colinus virginianus) at specific ambient temperatures (Ta). 2. No significant change in body temperature occurred at any Ta tested, but metabolic heat production (H) increased from 42.17 W/m2 at Ta 35 degrees C to 102.89 W/m2 at Ta 10 degrees C. 3. Evaporative heat loss (E) increased approximately two-fold from Ta 10-35 degrees C, with E/H increasing exponentially over the same temperature range. 4. No significant change in thermal insulation occurred from Ta 10-30 degrees C. 5. Combined convective and radiative heat transfer for the bobwhite was 2.96 W/m2 X C from Ta 10-35 degrees C.     

Energy and water conservation in frozen vs. supercooled larvae of the goldenrod gall fly, Eurosta solidaginis (fitch) (Diptera: Tephritidae)

Insects that tolerate severe cold during winter may either supercool or tolerate ice forming within the tissues of the body. To compare the relative advantages of freezing and supercooling, we measured rates of CO(2) production and water loss in frozen and supercooled goldenrod gall fly larvae (Eurosta solidaginis). As an important first step, we measured the time required for ice content and metabolic rate to stabilize upon freezing. Ice content stabilized after only three hours of freezing at -5 degrees C, whereas CO(2) production required 12 hours to stabilize. Subsequent experiments found that freezing greatly reduced both water loss and metabolic rate. Comparisons of supercooled and frozen larvae at -5 degrees C indicated that CO(2) production fell 47% with freezing and water loss decreased 35%. As temperature decreased to -10 and -15 degrees C, CO(2) production fell exponentially and was no longer detectable at -20 degrees C with our measurement system. Our results demonstrate that freezing significantly reduces energy consumption during the winter and may therefore improve winter survival and spring fecundity. The advantages of freezing over supercooling would drive selection toward insect freeze tolerance and also toward higher supercooling points to increase the duration of freezing each winter.     

Enhanced photo-H2 production of R. faecalis RLD-53 by separation of CO2 from reaction system

The effect of different gases, CO(2) concentration, and separation of CO(2) from reaction system on photo-fermentation H(2) production was investigated by batch culture in this study. Experimental results showed that different gases (Ar,N(2),CO(2), and air) as gas phase have obviously affected on photo-H(2) production and a high concentration of CO(2) can inhibit the growth and H(2) evolution of Rhodopseudomonas faecalis RLD-53. When CO(2) concentration at 5%, cell increased most rapidly the specific growth rate of 0.489 g/l/h and the specific growth rate fell to be 0.265 g/l/h when CO(2) concentration at 40%. However, the growth of RLD-53 at CO(2) concentration of 60-100% was almost completely inhibited. At CO(2) concentrations of 5% and 10%, the maximum H(2) yield was 2.54 and 2.59 mol-H(2)/mol acetate, respectively, and it was similar with the control (2.61 mol-H(2)/mol acetate). H(2) not produced when CO(2) concentration at 60-100%. In conclusion, separation of CO(2) from reaction system can stimulate H(2) production in the entire photo-H(2) production process and H(2) yield increased about 12.8-18.85% than the control.     

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.     

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.     

Interaction of acetogens and methanogens in anaerobic freshwater sediments

Anaerobic decomposition processes in the profundal sediments of Blelham Tarn (English Lake District) are often limited during late summer by the input of organic carbon. The concentration of acetate in the interstitial water fell from about 100 microM (immediately after sedimentation of the spring diatom bloom) to a relatively constant value of about 20 microM in late summer, during which acetate utilization appeared to be balanced by production. Addition of chloroform and molybdate caused an accumulation of cold acetate in large sediment cores and of [14C]acetate in small cores to which [14C]bicarbonate had been added. In both cases chloroform caused the greater accumulation, implying that acetoclastic methanogens were the more active consumers. The conversion of 14CO2 to [14C]acetate was inversely related, with depth, to its conversion to 14CH4. Methanogenesis from CO2 decreased during late summer, whereas acetogenesis and acetoclastic methanogenesis increased over the same time period. The production of acetate from CO2 was generally equivalent to less than 10% of the acetate carbon utilized but could be as high as 25% of that value. Hydrogen consumption by acetogens could be as high as 50% of that utilized in methanogenesis. The role of acetogenic bacteria in anaerobic processes may therefore be of greater significance in lakes such as Blelham Tarn than in more eutrophic systems.     

Interaction of acetogens and methanogens in anaerobic freshwater sediments.

Anaerobic decomposition processes in the profundal sediments of Blelham Tarn (English Lake District) are often limited during late summer by the input of organic carbon. The concentration of acetate in the interstitial water fell from about 100 microM (immediately after sedimentation of the spring diatom bloom) to a relatively constant value of about 20 microM in late summer, during which acetate utilization appeared to be balanced by production. Addition of chloroform and molybdate caused an accumulation of cold acetate in large sediment cores and of [14C]acetate in small cores to which [14C]bicarbonate had been added. In both cases chloroform caused the greater accumulation, implying that acetoclastic methanogens were the more active consumers. The conversion of 14CO2 to [14C]acetate was inversely related, with depth, to its conversion to 14CH4. Methanogenesis from CO2 decreased during late summer, whereas acetogenesis and acetoclastic methanogenesis increased over the same time period. The production of acetate from CO2 was generally equivalent to less than 10% of the acetate carbon utilized but could be as high as 25% of that value. Hydrogen consumption by acetogens could be as high as 50% of that utilized in methanogenesis. The role of acetogenic bacteria in anaerobic processes may therefore be of greater significance in lakes such as Blelham Tarn than in more eutrophic systems.     

Ambient thermal conditions and thermoregulatory mechanisms in fever in rabbits

At ambient temperatures 10 degrees C, 20 degrees C, 30 degrees C, and 40 degrees C the influence of heat dissipation on the thermoregulatory mechanisms in rabbits with fever was investigated. Temperature of the brain (TBr-accuracy +/- 0.05 degree C) temperature of the nasal mucosa (TN) and temperature of the ear pinna (TAU-accuracy +/- 0.5 degree C) were measured in freely moving rabbits. Changes of conditions of heat dissipation were produced by: preventing heat dissipation by convection and radiation by putting ear-pads on the ear pinnae, high humidity of air for blocking of heat loss through evaporation, and facilitation of heat dissipation through shearing of the fur. The changes of the ambient thermal conditions as well as of the ability of heat dissipation were followed by changes in the dynamics of functions of the remaining (effective) thermoregulatory mechanisms in the rabbits. Thus despite changed thermal conditions of the environment, the TBr of the rabbits with fever was stabilized at a similar level.     

Carbon dioxide and pH effects on temperature-sensitive and -insensitive hypothalamic neurons.

The preoptic-anterior hypothalamus (POAH) controls body temperature, and thermoregulatory responses are impaired during hypercapnia. If increased CO(2) or its accompanying acidosis inhibits warm-sensitive POAH neurons, this could provide an explanation for thermoregulatory impairment during hypercapnia. To test this possibility, extracellular electrophysiological recordings determined the effects of CO(2) and pH on the firing rates of both temperature-sensitive and -insensitive neurons in hypothalamic tissue slices from 89 male Sprague-Dawley rats. Firing rate activity was recorded in 121 hypothalamic neurons before, during, and after changing the CO(2) concentration aerating the tissue slice chamber or changing the pH of the solution bathing the tissue slices. Increasing the aeration CO(2) concentration from 5% (control) to 10% (hypercapnic) had no effect on most (i.e., 69%) POAH temperature-insensitive neurons; however, this hypercapnia inhibited the majority (i.e., 59%) of warm-sensitive neurons. CO(2) affected similar proportions of (non-POAH) neurons in other hypothalamic regions. These CO(2) effects appear to be due to changes in pH since the CO(2)-affected neurons responded similarly to isocapnic acidosis (i.e., normal CO(2) and decreased pH) but were not responsive to isohydric hypercapnia (i.e., increased CO(2) and normal pH). These findings may offer a neural explanation for some heat-related illnesses (e.g., exertional heat stroke) where impaired heat loss is associated with acidosis.     

Heat production, blood flow, O2 uptake and CO2 output in the secretary process of the dog submandibular gland (author's transl)

1. Under normal circulation of the dog submandibular gland, the electrical stimulation induced a massive salivary secretion (about 0.35 ml . min-1.g-1 gland weight) and an increase in the glandular temperature (about 0.2 degrees C). The heat production was calculated of about 60 mW.g-1. 2. Clamping of the glandular artery made both of secretion and heat production to be transient. The early peak of secretion was about 0.12 ml.min-1.g and that of heat production was 7 approximately 10mW,g-1. Then each 1 ml secretion followed about 4.6 J heat production. 3. Under constant blood flow in the glandular circulation, the secretory process was divided clearly into 2 phases of peak and plateau. The glandular temperature increased about 0.12 degrees C with an early temperature drop. In the secretory plateau phase, the secretary rate was about 0.043 ml.min-1.g-1, the heat production was about 5 approximately 7 mW.g-1 and each 1 ml secretion caused about 8.2 J heat production. 4. The rate of oxygen uptake was about 20.9 microl.min-1g-1 at the resting state. The maximum during secretion was about 192 microliter.min-1.g-1. THe half time of the recovery process of O2 uptake tended slightly longer than that of heat production. 5. THe rate of CO2 output was about 21.8 microliter.min-1.g-1 at resting. The maximum during secretion was about 142 microliter.min-1.g-1 R. Q. were about 1 at resting and about 0.74 under secretion.     

Effect of locomotor respiratory coupling on respiratory evaporative heat loss in the sheep.

During galloping, many animals display 1:1 coupling of breaths and strides. Locomotor respiratory coupling (LRC) may limit respiratory evaporative heat loss (REHL) by constraining respiratory frequency (f). Five sheep were exercised twice each, according to a five-step protocol: 5 min at the walk, 5 min at the trot (trot1), 10 min at the gallop, 5 min at the trot (trot2), and 5 min at the walk. Rectal temperature (T(re)), stride frequency, f, REHL, and arterial CO(2) tension and pH were measured at each step. Tidal volume (VT) was calculated. LRC was observed only during galloping. The coupling ratio remained at 1:1 while VT increased continuously during galloping, causing REHL to increase from 2.9 +/- 0.2 (SE) W/kg at the end of trot1 to a peak of 5.3 +/- 0.3 W/kg. T(re) rose from 39.0 +/- 0.1 degrees C preexercise to 40.2 +/- 0.2 degrees C at the end of galloping. At the gallop-trot2 transition, VT fell and f rose, despite a continued rise in T(re). Arterial CO(2) tension fell from 36.5 +/- 1.1 Torr preexercise to 31.8 +/- 1.4 Torr by the end of trot1 and then further to 21.5 +/- 1.2 Torr by the end of galloping, resulting in alkalosis. In conclusion, LRC did not prevent increases in REHL in sheep because VT increased. The increased VT caused hypocapnia and presumably elevated the cost of breathing.     

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.     

Epithelium-dependent regulation of airways smooth muscle function. A histamine-nitric oxide pathway.

The airway epithelium is responsible for the production of a number of arachidonic acid and non-prostanoid inhibitory factors. Epithelium synthesises nitric oxide (NO) which may be important in regulating the function of airways smooth muscles. We studied in vitro the effect of histamine (100 nM-100 microM) which increases the NO release on rabbit airway smooth muscles induced by 80 mM KC1 in the presence or not of 10(-5) Methylene blue (MB) (inactivator of guanylate cyclase) or N(G)-monomethyl L-arginine (L-NMMA), a NOS inhibitor. All experiments were done in tracheal muscle strips from 28 rabbits with epithelium and after epithelium removal. The additional use of histamine (1 microM) on KC1 contraction induced a relaxation of 10% of the initial contraction. The additional use of L-NMMA decreased the relaxation to 5% of initial contraction. MB rather than L-NMMA increased the contraction significantly (p<0.01). Epithelium removal increased the contraction induced by KC1 (80 mM) and histamine (1 microM) by about 30% (p<0.001). NO release especially from epithelium regulates the airways smooth muscle functions. Damage to the epithelium may contribute to an increase in airways sensitivity, observed in asthma.     

Arginine vasopressin does not mediate heat loss in the tail of the rat

It has been reported that hypothermia induced by arginine vasopressin (AVP) is brought about by a coordinated response of reduced thermogenesis in brown adipose tissue (BAT) and increased heat loss through the tail of rats. However, it is well known that AVP is one of the strongest peripheral vasoconstrictors. Whether the AVP-induced hypothermia is associated with an increase in heat loss through the tail is questionable. Therefore, the present study assessed the relationship between the effects of AVP on tail skin temperature and the induced hypothermic response, and to determine if peripheral AVP administration increases heat loss from the tail. Core, BAT and tail skin temperature were monitored by telemetry in male Sprague–Dawley rats before and after intraperitoneal administration of AVP or vasopressin receptor antagonist. We also analyzed simultaneously of the time-course of AVP-induced hypothermic response and its relationship with changes in BAT temperature, and effect of AVP on grooming behavior. The key observations in this study were: (1) rats dosed with AVP induced a decrease in heat production (i.e., a reduction of BAT thermogenesis) and an increase of saliva spreading for evaporative heat loss (i.e., grooming behavior); (2) AVP caused a marked decrease in tail skin temperature and this effect was prevented by the peripheral administration of the vasopressin V1a receptor antagonist, suggesting that exogenous AVP does not increase heat loss in the tail of rats; (3) the vasopressin V1a receptor antagonist could elevate core temperature without affecting tail skin temperature, suggesting that endogenous AVP is involved in suppression of thermogenesis, but not mediates heat loss in the tail of rats. Overall, the present study does not support the conclusion of previous reports that AVP increased tail heat loss in rats, because AVP-induced hypothermia in the rat is accompanied by a decrease in tail skin temperature. The data indicate that exogenous AVP-induced hypothermia attributed to the suppression of thermoregulatory heat production and the increase of saliva spreading for evaporative heat loss.     

Immunoglobulin E anaphylaxis in rabbits: mechanisms of pulmonary resistance and compliance changes

Factors causing changes in pulmonary resistance and dynamic compliance with immunoglobulin (Ig) E anaphylaxis in spontaneously breathing rabbits were assessed in ventilated rabbits using tantalum bronchography and wet-to-dry wt ratios. Ventilated rabbits demonstrated changes in resistance and compliance similar to spontaneously breathing rabbits. Chlorpheniramine pretreatment prevented increases in resistance but not decreases in compliance. Anaphylaxis constricted small (less than 1 mm) airways 20.9 +/- 16.0% (mean +/- SD) and intermediate (between 1 and 3 mm) airways 21.8 +/- 19.8%. Chlorpheniramine (10 mg/kg) prevented small airway changes and attenuated those in intermediate airways. Chlorpheniramine prevented histamine-induced constriction of small (23.6 +/- 15.7%) and intermediate (17.6 +/- 15.0%) airways. Lung wet-to-dry wt ratios were unchanged. Changes in resistance and compliance during rabbit IgE anaphylaxis are not due to changes in tidal volume or frequency. Histamine, via H1 receptors, is the principal mediator of pulmonary resistance increases but not dynamic compliance reductions. Chlorpheniramine-sensitive increases in resistance are caused by constrictions of intermediate and small airways, whereas the chlorpheniramine-resistant decrease in compliance is not caused directly by constriction of the smallest measurable airways (0.25 mm) or changes in lung water.     

Heat and water flux in the intrathoracic airways and exercise-induced asthma

To explore the relationship between the flux of heat and water within the respiratory tract during exercise and recovery to the development of exercise-induced asthma (EIA), we recorded airstream temperature at multiple points throughout the tracheobronchial tree in 10 normal and 10 asthmatic subjects before, during, and after cycle ergometry. In both groups, the intra-airway temperature fell progressively as ventilation increased, and there were no significant differences between the thermal profiles of the two populations at rest or during exercise. Calculation of water losses and the osmolality of the airway surface fluid failed to demonstrate significant airway drying in either group. With cessation of the work load, the airstream temperature increased abruptly, rising two times more rapidly in the asthmatics than the normals. Since the major source of heat in these experiments is the bronchial circulation, our findings suggest a reaction sequence consisting of vasoconstriction and airway cooling during exercise followed by a rapid resupply of heat when exercise ceases. The latter may cause the hyperplastic capillary bed in the airways of asthmatics to develop an exaggerated rebound hyperemia which may lead to airway edema and EIA.     

Cyclic gas exchange in the giant burrowing cockroach, Macropanesthia rhinoceros: effect of oxygen tension and temperature

The giant burrowing cockroach, Macropanesthia rhinoceros, is endemic to north-eastern Australia and excavates a permanent burrow up to 1m deep into soil. Using flow-through respirometry, we investigated gas exchange and water loss at three different oxygen tensions (21%, 10% and 2% at 20 degrees C) and temperatures (10, 20 and 30 degrees C at 21% oxygen). M. rhinoceros employ cyclic gas exchange (CGE) making the species by far the largest insect known to engage in discontinuous ventilation. CGE featured rhythmic bursts of CO(2) dispersed among inter-burst periods of reduced output. CGE was most commonly observed at 20 degrees C and degraded at <10% oxygen. Mild hypoxia (10% oxygen) resulted in a lengthening of the burst period by approximately two-fold; this result is complementary to oxygen consumption data that suggests that the burst period is important in oxygen uptake. When exposed to severe hypoxia (2% oxygen), CGE was degraded to a more erratic continuous pattern. Also, during severe hypoxia, total water loss increased significantly, although CO(2) release was maintained at the same level as in 21% oxygen. During CGE, an increase in temperature from 10 to 20 degrees C caused both water loss and CO(2) output to double; from 20 to 30 degrees C, CO(2) output again doubled but water loss increased by only 31%.     

Airway responsiveness: role of inflammation, epithelium damage and smooth muscle tension

The purpose of this study was the effect of epithelium damage on mechanical responses of airway smooth muscles under different resting tension. We performed acetylcholine (ACh) (10(-5) M)-induced contraction on tracheal strips from 30 rabbits in five groups (0.5, 1, 1.5, 2 and 2.5 g) before and after epithelium removal. At low resting tension (0.5-1.5 g), the epithelium removal decreased the ACh-induced contractions. At 2 g resting tension, the epithelium removal increased the ACh-induced contractions of airways with intact epithelium about 20%. At 2.5 g resting tension, the elevation of contraction is about 25% (P<0.01). Consequently, after epithelium loss, the resting tension determines the airway smooth muscles responsiveness. In asthma, mediators such as ACh act on already contracted inflammatory airways, which results in additional increase of contraction. In contrast, low resting tension, a condition that simulates normal tidal breathing, protects from bronchoconstriction even when the epithelium is damaged.