Temperature effects on CO2-sensitive intrapulmonary chemoreceptors in the lizard, Tupinambis nigropunctatus

Body temperature (Tb) effects on CO2 responses of 17 intrapulmonary chemoreceptors (IPC) were investigated in 9 anesthetized (pentobarbital; 30 mg/kg) and unidirectionally ventilated tegu lizards (Tupinambis nigropunctatus). At 30 degrees C, all IPC (n = 15) had a stable discharge pattern. At 20 degrees C, IPC discharge (n = 14) was stable at high PCO2 but irregular at low PCO2 and often (10/14) consisted of bursts of activity separated by one or more seconds of quiescence. Responses of IPC to static and dynamic changes in PCO2 were quantified at both Tb and the discharge rate vs PCO2 response curves were compared. Static discharge frequency (fSTAT) decreased as PCO2 increased at both Tb. At 20 degrees C: (1) fSTAT was diminished at all PCO2 levels relative to 30 degrees C; and (2) the slope of the fSTAT vs PCO2 relationship was markedly attenuated. The Q10 was 3.7 +/- 0.5 and was independent of PCO2. The peak discharge associated with a step decrease in PCO2 (dynamic response; fDYN) also decreased as PCO2 increased. At 20 degrees C: (1) fDYN was diminished at all PCO2 levels relative to 30 degrees C; but (2) the slope of the fDYN vs PCO2 relationship was similar at both Tb. The Q10 was 2.6 +/- 0.3 and was significantly less than the Q10 of fSTAT (P less than 0.05). Acute changes in Tb exert large effects on the CO2 response and discharge pattern of IPC; these effects on IPC may be important in ventilatory control at different Tb in lizards.     

Effects of intrapulmonary CO2 and airway pressure on pulmonary vagal afferent activity in the alligator

The effects of airway CO2 and pressure on pulmonary vagal afferent fibers were studied in seven anesthetized alligators Alligator mississippiensis, at room temperature (24 degrees C). Of 49 receptors which fired in phase with ventilation, 13 behaved like mammalian rapidly adapting pulmonary stretch receptors, 19 like mammalian slowly adapting pulmonary stretch receptors (PSR), and 17 like avian intrapulmonary CO2-sensitive chemoreceptors (IPC). PSR and IPC were positively localized to the lung by punctate stimulation or response to airway CO2 changes during pulmonary artery occlusion. PSR discharge frequency (fPSR) was measured at airway pressures (Paw) from 0 to 15 cm H2O at FICO2 = 0.01 in 14 receptors. fPSR increased in all receptors throughout the range of Paw studied. In 13 PSR, increasing FICO2 from 0.01 to 0.07 decreased fPSR 23 +/- 13% (+/- SEM) at Paw = 2 cm H2O and 14 +/- 7% at 15 cm H2O. IPC discharge frequency (fIPC) decreased as FICO2 increased and most discharged less than 1 sec-1 at FICO2 = 0.03. In 7 IPC at FICO2 = 0.01, increasing Paw from 2 to 15 cm H2O increased fIPC 17 +/- 5% after pulmonary artery occlusion demonstrating some mechanosensitivity in alligator IPC. Although both IPC and PSR showed mechanosensitivity and CO2-sensitivity, the two receptor types were distinct. PSR were 13 times more sensitive to Paw changes than IPC and IPC were 14 times more sensitive to FICO2 changes than PSR. We did not find any receptors with intermediate CO2- or mechanosensitivities that could represent a transitional form of receptor. These results predict that IPC and PSR may have different roles in reflex ventilatory control.     

Effects of vagotomy on ventilatory responses to CO2 in alligators.

Reptiles increase ventilation during hypercapnia at a constant temperature. In this study, the contributions of vagal vs non-vagal receptors to CO2 ventilatory responses were investigated in 16 sedated Alligator mississippiensis (25 mg/kg pentobarbital; 3 days prior to data collection). Four animals served as controls to assess the effects of time and/or anesthetic drift on ventilation and blood gases; significant ventilatory drift was not detected during the observation period. The effects of bilateral vagotomy on CO2 ventilatory responses were determined during spontaneous breathing (n = 6) and unidirectional ventilation (UDV; n = 6) at two body temperatures (Tb = 30 and 20 degrees C). Resting PaCO2, minute ventilation (VI), tidal volume (VT) and breathing frequency (f) were elevated at 30 degrees C relative to 20 degrees C in spontaneously breathing alligators. Increasing inspired CO2 to 5% increased PaCO2, f, VT and VI at both levels of Tb. Ventilatory sensitivity to CO2 (S = delta VI/delta PaCO2) was higher at 30 degrees C with a temperature coefficient (Q10) of 2.3. Vagotomy increased PaCO2 and VT, decreased f and had no effect on VI at either Tb. After vagotomy, hypercapnia had no effects on ventilation. When CO2 feedback loops were opened by UDV at a high flow rate (greater than 2 L/min), Tb had no effects on ventilatory efforts at constant PCO2, but hypercapnia significantly increased f, VT and VI. S was variable with a Q10 of 2.1. After vagotomy, a significant CO2-ventilatory response remained during UDV, but S was unaffected by Tb (Q10 = 0.8). The results indicate that non-vagal chemoreceptors contribute to CO2 ventilatory responses in alligators, although their contribution following vagotomy is evident only during unidirectional ventilation. Although tentative, the data also suggest that CO2-sensitive vagal receptors may be necessary for the temperature dependency of S.     

Effects of hypercapnia on phrenic and stretch receptor responses to lung inflation

To determine if hypercapnia and reflex bronchoconstriction attenuate lung inflation effects on ventilatory activity by indirect effects on intrapulmonary stretch receptors (PSR), phrenic nerve activity and single unit PSR were monitored at controlled levels of static airway pressure (Paw) and arterial PCO2 in 15 anesthetized dogs. Paw in a vascularly isolated lung was varied between 2 and 14 cm H2O at levels of PaCO2 between 35 and 85 mm Hg. PSR activity (n = 38) in fine strands dissected from an otherwise intact vagus nerve and the integrated phrenic neurogram were recorded. The response to Paw varied from one PSR to another, but was consistent in a given unit; PaCO2 had no consistent effect on individual responses. Selected PSR (n = 15) were averaged to yield a population response to Paw; the selection criteria were: phrenic activity responded briskly to Paw and measurements were made at three levels of PaCO2. Average PSR discharge increased linearly with Paw but was unaffected by PaCO2. On the other hand, phrenic burst frequency decreased as Paw increased and hypercapnia attenuated the slope of this relationship. These results suggest that effects on the relationship between PSR activity and Paw cannot account for attenuation of the relationship between phrenic frequency and Paw in hypercapnia. The effect of PaCO2 on the phrenic frequency vs Paw relationship probably arises from integrative mechanisms in the central nervous system.     

Acid-base state and intermittent breathing in the torpid bat, Eptesicus fuscus.

The effects of intermittent breathing on acid-base state and blood gases were characterized in the torpid bat, Eptesicus fuscus, during steady-state torpor between body temperatures (Tb) of 5 and 37 degrees C. Arterial blood samples were taken from indwelling catheters without disturbing the torpid state. Arterial pH (pHa) of samples taken without knowledge of ventilatory state rose by 0.15 units from 37 to 5 degrees C with a delta pHa/delta Tb slope over this range of -0.0055 U/degrees C. However, at and below Tb = 20 degrees C, Eptesicus fuscus breathes intermittently with typical apneic periods of 40-150 min and 4-12 min at 10 and 20 degrees C, respectively. Samples taken at the end of a ventilatory bout and near the end of an apneic period at Tb = 20 degrees C revealed cyclic changes in pH (from 7.49 +/- 0.02 to 7.34 +/- 0.01), PO2 (from 96.6 +/- 3.4 to 30.8 +/- 3.9 Torr), and PCO2 (28.2 +/- 1.4 to 45.9 +/- 1.5 Torr). Between 10 and 37 degrees C, end-ventilatory pHa varied inversely with temperature with a delta pHa/delta T slope of -0.011 U/degrees C. Because intermittent breathing is common to many animals during hibernation, these results demonstrate the importance of coordinating blood sampling with ventilatory state for a reliable interpretation of acid-base regulation under these conditions.     

Effects of changes in tidal volume on avian intrapulmonary chemoreceptor discharge

It has been suggested that avian intrapulmonary CO2-sensitive receptors (IPC) may be capable of monitoring the rate and extent of CO2 washout from the lung during spontaneous breathing. The purpose of this study was to analyse IPC discharge activity (using computerised bin-averaging and counting techniques) in spontaneously breathing domestic fowl when VT was elevated from resting levels. This was accomplished by administration of almitrine (2 mg X kg-1 i.v.), a respiratory stimulant drug that has been shown to have a specific long-lasting stimulatory action on carotid body chemoreceptors. Unanaesthetized decerebrate chickens were tracheotomized and single unit activity was recorded from 14 IPC. When VT progressively increased following administration of almitrine (with little or no change in TI or TE), IPC activity increased in a linear relationship with the increased VT. IPC activity in expiration was also increased, and the delay period before the onset of IPC discharge in inspiration was shortened. It is concluded that IPC discharge is increased when VT is elevated in the spontaneously breathing chicken and hence the IPC are capable of monitoring the extent of each ventilatory effort. It is well known that IPC have strong inhibitory effects on ventilatory motor output and conceivably they could originate reflexogenic information to the respiratory centres in response to intrapulmonary PCO2 changes. The latter could arise from changes in CO2 delivery by the mixed venous blood or from changes in the extent of CO2 washout with each breath.     

Response of intrapulmonary chemoreceptors in the duck to changes in PCO2 and pH.

We have estimated the relative importance of changes in blood PCO2 and pH in determining activity of intrapulmonary chemoreceptors (IPC) in the unidirectionally ventilated duck. The response of single unit vagal afferents from IPC to changing lung gas PCO2 was tested before and after changing blood pH by intravenous infusion of NaHCO3. Using multiple linear regression analysis, we calculated how much of the change in IPC activity for a given change in PCO2 was due to the changing PCO2 at constant pH (CO2 sensitivity) or to the change in pH concomitant with the change in PCO2 (H+ sensitivity). For 10 IPC, the CO2 sensitivity was on the average 2.3 times larger than the H+ sensitivity. Changes in pH as well as PCO2 of lung blood should be considered in assessing the role of IPC in control of breathing.     

Interaction of temperature with extra- and intrapulmonary chemoreceptor control of ventilatory movements in the awake chicken

Several studies in artificially ventilated, anesthetized birds with opened thoracoabdominal cavities have shown that intrapulmonary chemoreceptors (IPC) sensitive to CO2 contribute to the control of ventilatory movements. Increasing colonic temperature (Tc) has been shown to increase depth and decrease frequency of ventilatory movements if PaCO2 is held constant at less than 35 torr in awake and anesthetized, artificially ventilated cockerels. The relative importances, though, of IPC and of extrapulmonary CO2-sensitive chemoreceptors (EPC) in controlling ventilation in the awake or hyperthermic bird is unknown. We dissociated the PCO2 affecting IPC and EPC in awake cockerels by ligating the left pulmonary artery, denervating the IPC in the right lung and artificially ventilating each lung separately. We found, that at constant PaCO2, ventilatory movements increased in depth and decreased in frequency with: (1) increasing PICO2 to the innervated, non-perfused lung (PipcCO2); and (2) increasing Tc. Similar responses were observed with increasing PaCO2 or Tc during constant PipcCO2. Multiple regression analyses show that IPC and EPC have about equal controlling influences on ventilatory movements in the awake and hyperthermic cockerel.     

Discharge of pulmonary rapidly adapting stretch receptors during HFO ventilation.

High-frequency oscillatory ventilation (HFOV) has been shown to stimulate slowly adapting pulmonary stretch receptors (PSR) and thereby to inhibit spontaneous breathing, i.e. HFOV prolongs expiration or even elicits normocapnic apnea. However, during HFOV respiratory effects possibly mediated by pulmonary rapidly adapting receptors (RAR) have also been observed, e.g., diaphragmatic activation or augmented breaths. Therefore, we analyzed HFOV-induced changes in RAR activity in anaesthetized rabbits by mean of single fibre preparations of vagal RAR afferents. HFOV was applied in several combinations of airway pressure (Paw) and oscillation frequency (fOsc). In the sample of 60 RAR fibres prepared in 20 rabbits we found a wide spectrum of discharge patterns during HFOV. The inspiratory discharge rate during HFOV was increased in 38, decreased in 10, and unchanged in 12 RAR. The expiratory discharge rate was increased in 34, decreased in 17, and unchanged in 9 RAR. The effects of gradually changing Paw or of fOsc during HFOV were different in different fibres. In 17 fibres both inspiratory and expiratory discharge rates rose with increasing Paw during HFOV, whereas 19 fibres were not affected by increasing Paw. In some fibres either the inspiratory (12) or the expiratory (9) activity was inhibited in proportion to increasing Paw. From these results we conclude, that (a) the changes of RAR activity during HFOV are heterogeneous and the reflex effects of RAR stimulation may be balanced by RAR with decreased activity; (b) this heterogeneity of RAR discharge patterns explains the dominancy in the control of breathing during HFOV of the homogeneously stimulated PSR; and (c) depending on HFOV ventilatory parameters used the overall RAR stimulation may be strong enough to overrule the inspiration-inhibiting effects of PSR.     

Sodium bicarbonate infusion increases discharge frequency of intrapulmonary chemoreceptors only at high CO2

We felt that earlier determinations of independent effects of extracellular pH and PCO2 on intrapulmonary chemoreceptors (IPC) discharge frequency were difficult to analyze because they used perfused lungs, and ventilation-perfusion changes among parabronchi could not be controlled. We decided to repeat these studies in non-perfused lungs. We cannulated both extrapulmonary bronchi of 10 thoracotomized Pekin ducks anesthetized with sodium pentobarbital (25-35 mg/kg) and unidirectionally ventilated each lung. The perfused right lung maintained gas exchange while the non-perfused left lung received 0.6 L/min of CO2 mixed in air. We recorded the discharge frequency of one IPC per duck at various PCO2, re-established circulation, and infused 3.0 mmol/kg of sodium bicarbonate intravenously. After 15 min, discharge frequencies were again measured from the same IPC in the nonperfused lung. The slopes and intercepts of discharge frequencies vs ln PCO2 relationship were depressed in six IPC, increased in two IPC and not significantly affected in two IPC. Arterial pH was increased significantly (0.11 unit) at 38 Torr arterial PCO2. We conclude that acutely increased extracellular sodium bicarbonate affects IPC discharge only by depressing sensitivity of most IPC to PCO2 and does not have an independent effect through pH.     

The ventilatory recruitment threshold for carbon dioxide

We report our initial experience with a technique with which the chemoresponsiveness of the respiratory controller can be characterized in terms of an inspiratory on-switch threshold to CO2. After suppression of phasic respiratory muscle activity by mechanical ventilation, a CO2 recruitment threshold (PCO2RT) was defined as the lowest alveolar CO2 tension at which CO2 supplementation to inspired gas caused a reappearance of inspiratory efforts. Because PCO2RT can be determined in the absence of a mechanical load on the ventilatory pump, respiratory system mechanics and inspiratory muscle function should not influence the measurement itself. Thus, this technique may be helpful to study ventilatory requirements and load responses in critically ill patients with respiratory failure. We have shown that inspiratory muscle recruitment can be equally well-inferred from changes in the airway pressure and flow tracings during mechanical ventilation, from the pattern of chest wall displacement, and from the integrated diaphragm electromyogram. Within a subject, PCO2RT is a reproducible measurement that is not influenced by ventilator settings and end-expiratory lung volume, provided that phasic respiratory muscle has been suppressed prior to CO2 supplementation. Details of the methodology, the likely determinants of PCO2RT, and the clinical utility of this technique are discussed.     

Middle cardiac nerve section alters ventilatory response to PaCO2 in the cockerel

To determine whether afferents in the middle cardiac nerves (MCN) contribute to extrapulmonary PaCO2 sensitivity, we did the following: we anesthetized six cockerels with sodium pentobarbital (25-35 mg/kg), and cannulated the cutaneous ulnar vein, and the carotid and brachial arteries. The thorax was opened and each lung unidirectionally ventilated from separate gas delivery systems. A ligature, which temporarily occluded blood flow, was placed around the right pulmonary artery. Both cardiac sympathetic nerves were cut, as well as the left vagus just above the level of the recurrent branch. We exposed the non-perfused right lung to 105 Torr PCO, to silence intrapulmonary chemoreceptors (IPC). We measured blood pressure, heart rate and ventilatory movements while the denervated left lung was used to fix PaCO2 at seven levels ranging from 7-140 Torr. As arterial PCO2 increased, ventilatory amplitude increased from 0.3 mm to 3.6 mm, while frequency decreased from 140 to 24 per min. After cutting the MCN, ventilatory movements were less responsive to PaCO2 changes. Ventilatory amplitude was 3.0 mm at the lowest PaCO2 and increased to 4.0 at the highest PaCO2. We conclude that: 1) when IPC discharge is low, afferents in the MCN inhibit ventilatory movements during hypocapnia, and 2) these afferents may contribute to systemic CO2 sensitivity.     

Oxygen consumption and acid-base balance during shallow hypothermia in the pigeon.

In pigeons, during shallow nocturnal hypothermia induced by food deprivation, body temperature falls to values between 35 degrees C and 38 degrees C. Body temperature, oxygen consumption, and arterial blood pH and PCO2 were recorded during the entrance into such nocturnal hypothermic periods. In vivo pH was kept constant, while in vivo PCO2 increased slightly during hypothermia. This caused the temperature-corrected value of pH (pH*, measured at 40 degrees C) to fall by -0.014 units/degrees C, and the total CO2-content to rise by 3.2 mM, an increase of 16%. These changes in the acid-base balance represent, in effect, a respiratory acidosis that closely parallels the normal buffer line for pigeons. Q10 values, relating oxygen uptake to body temperature, were higher than 4.0 at the very beginning of the entrance into hypothermia, indicating that the metabolic rate was actively inhibited. However, the present results do not indicate any relationship between the acidosis and the inhibition of the metabolic rate.     

Effects of temperature on the ventilatory response to inspired CO2 in unanaesthetized domestic fowl

The influence of raised environmental temperature on the respiratory response to CO2 in awake, spontaneously breathing domestic fowl was investigated. In terms of their effects on ventilation VE temperature and CO2 were additive and non-interactive, VE being approximately 1900 ml . min-1 greater at 33 +/- 1 degree C compared to 18 +/- 1 degree C, regardless of inspired CO2 partial pressure PICO2. Temperature had no effect on the slope of the relationship between VE and both arterial and clavicular air sac PCO2. Blood and clavicular sac PCO2 were regulated within 2-3 Torr of normal at PICO2 levels below approximately 20 Torr as a result of hyperventilation but PCO2 regulation began to fail at higher PICO2. Hypercapnia induced increases in respiratory frequency f at normal temperatures but decreases in f at 33 +/- 1 degree C. There was little change in f at 25 +/- 1 degree C. The ventilatory increase in response to CO2 at 18 +/- 1 degree C and 25 +/- 1 degree C could be described by a linear relationship between VE and tidal volume VT. However, respiration departed from this pattern at temperatures above the panting threshold (32-34 degrees C). These findings are discussed in the context of central and peripheral mechanisms which may be involved in the control of rate and depth of breathing.     

Aging effects on the interaction of hypercapnia and hypoxia as ventilatory stimuli

We measured ventilatory responses to progressive hypercapnia at two steady-state levels of oxygenation and to progressive hypoxia at two steady-state levels of CO2 in 10 elderly and 10 young individuals. Under hyperoxic conditions, the ventilatory response to progressive hypercapnia was not significantly different between age groups but, under hypoxic conditions, the response to hypercapnia was lower in the elderly group. The interaction of hypercapnic and hypoxic stimuli was greater among young persons as indicated by a higher ratio of the hypercapnic response slopes (hypoxic/hyperoxic); 1.48 +/- 0.19 versus 0.98 +/- 0.11, p less than .05. The ventilatory response to hypoxia at the lower CO2 level was significantly greater among elderly than among young adults but not significantly different between age groups at the higher CO2 level. The ratio of hypoxic response slopes (high PCO2/lower PCO2) was 1.56 +/- 0.17 among elderly participants and 3.14 +/- 0.63 among young participants (p less than .05). These results suggest that aging diminishes the multiplicative effect of hypercapnia and hypoxia as ventilatory stimuli.     

Changes in ventilation and breathing pattern produced by changing body temperature and inspired CO2 concentration in turtles

Respiratory minute ventilation (VE), breathing pattern, oxygen consumption (VO2) and arterial blood gases and pH were measured in freshwater turtles (Chrysemys picta) at 10, 20 and 30 degrees C while the animals breathed gases of varying CO2 concentration (FICO2 = 0, 2, 4, 6 and 8%). Increasing body temperature produced unequal increases in VE and VO2 such that VE/VO2 decreased. This relative hypoventilation led to a rise in PaCO2 and fall in pHa. Increasing FICO2 at all temperatures greatly elevated VE. The magnitude of this response increased with increasing temperature. Thus, paradoxically, there was an increase in both PaCO2 and CO2 sensitivity with increasing temperature. Increases in VE due to increases in temperature were primarily due to a shortening of the periods of breath holding. Although changes in VT contributed to changes in VE with increasing FICO2, the changes in f, due to shortening the periods of breath holding, contributed twice as much. In relative terms, increasing temperature had no effect on the CO2 response of any respiratory variable. Analysis of the data indicates that all changes which occurred in VE, PaCO2 and pHa with changes in body temperature can be explained by equal Q10 effects of roughly two on both metabolic rate and ventilatory sensitivity to changes in PaCO2.     

Effect of temperature on the CO2 sensitivity of avian intrapulmonary chemoreceptors

We determined linear regressions of discharge frequency on ln PCO2 of 23 intrapulmonary chemoreceptors (IPC) from eight hyperthermic, adult cockerels. At low PCO2, IPC in hyperthermic cockerels discharged slower than IPC measured in euthermic cockerels; above 25 torr PCO2, however, they discharged faster than euthermic IPC. Thus, IPC were less sensitive to PCO2 during hyperthermia. We calculate that a 1 degree C increase in the temperature of the lung (TL) causes the slope of the linear regression of discharge frequency on ln PCO2 to be less negative by 1.5 +/- 0.5 imp (sec X ln PCO2)-1 and that, for any increase in TL above normal (41.5 degrees C), the average IPC discharge frequency equals (-10.7 + 1.5 (TL -41.5] X (ln (PCO2/25.0] + 3.7. This relationship may be partly responsible for the increased tidal volume and decreased respiratory frequency observed when body temperature increases during constant PaCO2.     

Pulmonary gas exchange during intermittent ventilation in the American alligator.

The present study characterized pulmonary gas exchange in the American alligator, Alligator mississipiensis during ventilation and apnea at a body temperature (Tb) of 25 degrees C. Pulmonary gas exchange parameters were measured on a breath-by-breath basis utilizing a computer-assisted data acquisition system. In addition, paired blood samples were analyzed from left and right atrium during ventilation and voluntary apneas (1, 2, 5 and 10 min). Measurements of lung PO2 and PCO2 indicated that as apnea progressed, CO2 flux into the lung decreased rapidly while O2 was continuously removed at a constant and steady rate. The reduction in VCO2 resulted in a decrease in R (less than 0.4). Blood gas measurements indicated that the pulmonary arterial-pulmonary venous PCO2 difference, (Ppa-Ppv)CO2 was 4.9 +/- 0.9 mmHg during ventilation, decreased and became negative within 2 min of apnea, reaching -3.9 +/- 0.6 mmHg after 10 min. It is postulated that during apnea the Haldane effect accounts for both the blood gas behavior across the lung and insures a continued CO2 flux into the lung during apnea.     

Blood acid-base status of an awake heterothermic rodent, Spermophilus tereticaudus

The desert ground squirrel Spermophilus tereticaudus is shown to show both reptilian style alphastat regulation and the pH-stat regulation typical of mammalian hibernation, depending upon the range of body temperature and the state of vigilance. Temperature corrected arterial pH and PCO2 of torpid squirrels (Tb 11-28 degrees C) were independent of Tb and about equal to euthermic values at 37 degrees C. Torpid squirrels show a progressive respiratory acidosis as Tb is lowered. In awake heterothermic squirrels (Tb 30-42.5 degrees C), blood acid-base status is like that of many ectothermic vertebrates: from 30 to 40 degrees C delta pHa/delta Tb was -0.0121, delta PaCO2/delta Tb was 1.057 and [HCO3-] remained about constant. Arterial blood from awake heterothermic squirrels measured at standard temperature (37 degrees C) showed no significant change with Tb, similar to blood undergoing anaerobic temperature changes in vitro. In vitro, the delta pH/delta T of blood of constant CCO2 was -0.014. Constant blood pH with change in Tb is thus not a general feature of mammalian acid-base regulation but appears in this species to be a feature of the respiratory and metabolic poise of torpor.     

Inspiratory muscle activity during pulmonary edema in anesthetized dogs.

Pulmonary edema is known to induce a rapid and shallow breathing pattern. However, its effects on the level and pattern of distribution of motor activity to the respiratory muscles is unclear. In the present study we evaluated the effect of oleic acid induced pulmonary edema on the electrical activity of the inspiratory muscles (costal and crural diaphragm and parasternal and external intercostal muscles) in the dog, and related it to the transdiaphragmatic pressure and ventilatory parameters over the course of CO2 rebreathing. Pulmonary edema, reflected by a 7.1 +/- 0.6 wet to dry ratio, decreased lung compliance by 57%, increased pulmonary shunt to 35%, and was associated with a rapid and shallow breathing pattern. When compared at equal levels of PCO2 during CO2 rebreathing before and during edema, ventilation and mean inspiratory flow were increased only at lower levels of hypercapnia and their responses to increasing levels of PCO2 were significantly diminished during edema. Transdiaphragmatic pressures were elevated during edema as compared to control values. The rate of rise of the electrical activity of all inspiratory muscles increased significantly during edema at all levels of PCO2. Peak activity, however, remained unchanged, due to shortening of the inspiratory duration. The EMG responses to progressive hypercapnia were not affected by edema. Pulmonary edema did not change the pattern of breathing and neural output to the inspiratory muscles in vagotomized dogs. We conclude that stimulation of pulmonary proprioreceptors during edema increases neural output to all inspiratory muscles. The neural response to hypercapnia is not altered by edema, and is additive to the vagal input. The ventilatory response to CO2 is blunted during severe edema, due to alterations in lung mechanics.