Postnatal maturation of ventilation and breathing pattern in kittens: influence of sleep

Ventilation and breathing pattern were studied in kittens at 1, 2, 3, 4, and 8 wk of life during quiet wakefulness (W), quiet sleep (QS), and active sleep (AS) with the barometric method. Tidal volume (VT), respiratory frequency (f), ventilation (VE), inspiratory time (TI), expiratory time (TE), mean inspiratory flow (VT/TI), and respiratory "duty cycle" (TI/TT) were measured. VT, VE, TI, TE, and VT/TI increased; f decreased and TI/TT remained constant during postnatal development in wakefulness and in both sleep states. No significant difference was observed between AS and QS for all the ventilatory parameters except TI/TT, which was greater in QS than in AS at 2 wk. VE was larger in W than in both AS and QS at all ages. This was mainly due to a greater f, TI/TT remaining constant. VT/TI, which represents an index of the central inspiratory activity, was larger in W than in sleep, VT not being significantly different whatever the stage of consciousness. The results of this study show that in the kitten 1) unlike in the adult cat, ventilation and breathing pattern are similar in QS and in AS; 2) in sleep, the central inspiratory drive appears to be independent of the type of sleep; and 3) in wakefulness, the increase of the central inspiratory activity could be related to important excitatory inputs.     

Effects of acute exposure to high altitude on ventilatory drive and respiratory pattern

To assess changes in ventilatory regulation in terms of central drive and timing, on exposure to high altitude, and the effects of induced hyperoxia at high altitude, six healthy normal lowland subjects (mean age 19.5 +/- 1.64 yr) were studied at low altitude (518 m) and on the first 4 days at high altitude (3,940 m). The progressive increase in resting expired minute ventilation (VE; control mean 9.94 +/- 1.78 to 14.25 +/- 2.67 l/min on day 3, P less than 0.005) on exposure to high altitude was primarily due to a significant increase in respiratory frequency (f; control mean 15.6 +/- 3.5 breaths/min to 23.8 +/- 6.2 breaths/min on day 3, P less than 0.01) with no significant change in tidal volume (VT). The increase in f was due to significant decreases in both inspiratory (TI) and expiratory (TE) time per breath; the ratio of TI to TE increased significantly (control mean 0.40 +/- 0.08 to 0.57 +/- 0.14, P less than 0.025). Mouth occlusion pressure did not change significantly, nor did the ratio of VE to mouth occlusion pressure. The acute induction of hyperoxia for 10 min at high altitude did not significantly alter VE or the ventilatory pattern. These results indicate that acute exposure to high altitude in normal lowlanders causes an increase in VE primarily by an alteration in central breath timing, with no change in respiratory drive. The acute relief of high altitude hypoxia for 10 min has no effect on the increased VE or ventilatory pattern.     

Human breathing patterns on mouthpiece or face mask during air, CO2, or low O2

Steady-state breathing patterns on mouthpiece and noseclip (MP) and face mask (MASK) during air and chemostimulated breathing were obtained from pneumotachometer flow. On air, all 10 subjects decreased frequency (f) and increased tidal volume (VT) on MP relative to that on MASK without changing ventilation (VE), mean inspiratory flow (VT/TI), or mean expiratory flow (VT/TE). On elevated CO2 and low O2, MP exaggerated the increase in VE, f, and VT/TE due to profoundly shortened TE. On elevated CO2, MASK exaggerated VT increase with little change in f. Increased VE and VT/TI were thus due to increased VT. During low O2 on MASK, both VT and f increased. During isocapnia, shortened TE accounted for increased f; during hypocapnia, increased f was related primarily to shortened TI. Thus the choice of a mouthpiece or face mask differentially alters breathing pattern on air and all components of ventilatory responses to chemostimuli. In addition, breathing apparatus effects are not a simple consequence of a shift from oronasal to oral breathing, since a noseclip under the mask did not change breathing pattern from that on mask alone.     

Effects of inspiratory resistive load on respiratory control in hypercapnia and exercise

Eight healthy young men underwent two separate steady-state incremental exercise runs within the aerobic range on a treadmill with alternating periods of breathing with no load (NL) and with an inspiratory resistive load (IRL) of approximately 12 cmH2O.1-1.s. End-tidal PCO2 was maintained constant throughout each run at the eucapnic or a constant hypercapnic level by adding 0-5% CO2 to the inspired O2. Hypercapnia caused a steepening, as well as upward shift, relative to the corresponding eucapnic ventilation-CO2 output (VE - VCO2) relationship in NL and IRL. Compared with NL, the VE - VCO2 slope was depressed by IRL, more so in hypercapnic [-19.0 +/- 3.4 (SE) %] than in eucapnic exercise (-6.0 +/- 2.0%), despite a similar increase in the slope of the occlusion pressure at 100 ms - VCO2 (P100 - VCO2) relationship under both conditions. The steady-state hypercapnic ventilatory response at rest was markedly depressed by IRL (-22.6 +/- 7.5%), with little increase in P100 response. For a given inspiratory load, breathing pattern responses to separate or combined hypercapnia and exercise were similar. During IRL, VE was achieved by a greater tidal volume (VT) and inspiratory duty cycle (TI/TT) along with a lower mean inspiratory flow (VT/TI). The increase in TI/TT was solely because of a prolongation of inspiratory time (TI) with little change in expiratory duration for any given VT. The ventilatory and breathing pattern responses to IRL during CO2 inhalation and exercise are in favor of conservation of respiratory work.(ABSTRACT TRUNCATED AT 250 WORDS)     

Breathing patterns during varied activities.

The level of ventilation attained and breathing patterns adopted during activity have important implications for the distribution and deposition of particles that are inhaled. However, breathing patterns and levels of ventilation adopted during specific physical activities are unknown. We used a noninvasive means of measuring ventilation in subjects performing a variety of activities (bicycling, arm ergometry, lifting, and pulling) during unencumbered (no mouthpiece) breathing and while breathing through a mouthpiece. Minute ventilation (VE), tidal volume (VT), inspiratory time (TI), and total breathing cycle time (TT) were measured initially both spirometrically and from body surface displacements. When a mouthpiece was used, VE and breathing patterns were significantly altered during all activities such that VE, VT, and TT increased by 16, 34, and 20%, respectively. This mouthpiece effect was attenuated at the higher levels of VE. A task dependency of breathing pattern was also noted such that there was much greater variability of VT and TI for a given VE during the lifting activity compared with bicycling (coefficient of variation for VT of 0.39 +/- 0.09 vs. 0.20 +/- 0.07, P less than 0.01; and for TI of 0.38 +/- 0.08 vs. 0.21 +/- 0.08, P less than 0.01). We conclude that a mouthpiece significantly alters breathing pattern during varied types and intensities of activities, and breathing patterns may differ significantly from one activity to another. When the total dose of particulates inhaled in the lung are assessed, the mouthpiece effect and activity effect on breathing pattern must be considered.     

Hyperpnoea and CO2 sensitivity of the respiratory centres during exercise

The aim of this study was to specify whether exercise hyperpnoea was related to the CO2 sensitivity of the respiratory centres measured during steady-state exercise of mild intensity. Thus, ventilation (VE), breathing pattern [tidal volume (VT), respiratory frequency (f), inspiratory time (TI), total time of the respiratory cycle (TTOT), VT/TI, TI/TTOT] and CO2 sensitivity of the respiratory centres determined by the rebreathing method were measured at rest (SCO2re) and during steady-state exercise (SCO2ex) of mild intensity [CO2 output (VCO2) = 20 ml.kg-1.min-1] in 11 sedentary male subjects (aged 20-34 years). The results showed that SCO2re and SCO2ex were not significantly different. During exercise, there was no correlation between VE and SCO2ex and, for the same VCO2, all subjects had very close VE values normalized for body mass (bm), regardless of their SCO2ex (VEbm0.75 = 1.44 l.min-1.kg-1 SD 0.10). A highly significant positive correlation between SCO2ex and VT (normalised for bm) (r = 0.80, P less than 0.01), TI (r = 0.77, P less than 0.01) and TTOT (r = 0.77, P less than 0.01) existed, as well as a highly significant negative correlation between SCO2ex and (normalised for bm-0.25) (r = -0.73, P less than 0.01). We conclude that the hyperpnoea during steady-state exercise of mild intensity is not related to the SCO2ex. The relationship between breathing pattern and SCO2ex suggests that the breathing pattern could influence the determination of the SCO2ex. This finding needs further investigation.     

Ventilatory response to fatiguing and nonfatiguing resistive loads in awake sheep

To study the changes in ventilation induced by inspiratory flow-resistive (IFR) loads, we applied moderate and severe IFR loads in chronically instrumented and awake sheep. We measured inspired minute ventilation (VI), ventilatory pattern [inspiratory time (TI), expiratory time (TE), respiratory cycle time (TT), tidal volume (VT), mean inspiratory flow (VT/TI), and respiratory duty cycle (TI/TT)], transdiaphragmatic pressure (Pdi), functional residual capacity (FRC), blood gas tensions, and recorded diaphragmatic electromyogram. With both moderate and severe loads, Pdi, TI, and TI/TT increased, TE, TT, VT, VT/TI, and VI decreased, and hypercapnia ensued. FRC did not change significantly with moderate loads but decreased by 30-40% with severe loads. With severe loads, arterial PCO2 (PaCO2) stabilized at approximately 60 Torr within 10-15 min and rose further to levels exceeding 80 Torr when Pdi dropped. This was associated with a lengthening in TE and a decrease in breathing frequency, VI, and TI/TT. We conclude that 1) timing and volume responses to IFR loads are not sufficient to prevent alveolar hypoventilation, 2) with severe loads the considerable increase in Pdi, TI/TT, and PaCO2 may reduce respiratory muscle endurance, and 3) the changes in ventilation associated with neuromuscular fatigue occur after the drop in Pdi. We believe that these ventilatory changes are dictated by the mechanical capability of the respiratory muscles or induced by a decrease in central neural output to these muscles or both.     

Transient changes in expiratory time during hypercapnia in premature infants

The transient ventilatory responses to hypercapnia were studied in nine healthy preterm infants. We administered 4% CO2 in air for at least 7 min during quiet sleep and measured frequency (f), inspiratory time (TI), expiratory time (TE), tidal volume (VT), and minute ventilation (VI). Frequency increased over the first 2 min of CO2 inhalation (P less than 0.05) and then decreased to control values (P less than 0.05). This response was secondary to changes in TE, which decreased over the first 2 min (P less than 0.05) and then returned to control values, whereas TI did not change. The late increase in TE was associated with an increased percent of breaths exhibiting retardation of expiratory flow (braking) (P less than 0.05). These breaths had longer TE than the breaths without braking (P less than 0.05). Exponential curves made to fit the increases in VI and VT revealed that only 67% of the infants reached 90% of steady state for both VI and VT over the 7-min study period. The time to 90% of steady state was always shorter for VI than VT (P less than 0.05) due to the transient changes in f. The results indicate that the transient changes of f in response to hypercapnia are secondary to changes in TE, which appear unique to human infants. We speculate that the expiratory braking that develops during the course of CO2 inhalation increases lung volume, resulting in prolongation of TE via mechanoreceptor-mediated reflexes.     

Effects of tonic vagal input on breathing pattern in newborn rabbits

Respiratory effects of positive and negative pressure breathing were studied in 1- and 4-day-old rabbit pups anesthetized with ketamine (50 mg/kg, im) and acepromazine (3 mg/kg, im). We recorded tidal volume (VT), tracheal pressure (Ptr), and integrated diaphragmatic EMG (DiEMG). Inspiratory (TI) and expiratory time (TE) were measured from the records of DiEMG. During breathing with increased Ptr by 1 or 2 cmH2O, VT, minute ventilation (VE), and respiratory rate (f) decreased. Changes in f relied on a TE prolongation. Neither DiEMG nor its rate of rise (DiEMGt) were affected. Except for VT decrease during positive Ptr, all other effects disappeared after vagotomy. Our results indicate that an increase in tonic vagal activity interacts with the mechanisms controlling TE and has no effect on depth and duration of inspiration. When Ptr decreased by 1 and 2 cmH2O, VE increased due to an increase in f. Increase in f relied on shortening of both TI and TE; the TE effect being more pronounced. DiEMG and DiEMGt also increased. Adverse effects of lung deflation and vagotomy strongly suggest that the respiratory reflex stimulation due to decrease in Ptr does not rely on inhibition of the slowly adapting stretch receptor activity. Therefore other excitatory vagal inputs must be responsible for this response. We propose two vagally mediated inputs: the irritant and/or the cardiac receptors.     

Effects of almitrine on respiration in unanesthetized newborn rabbits

We previously demonstrated that almitrine, a peripheral chemoreceptor stimulant, increased tidal volume (VT), expired minute ventilation (VE), and respiratory frequency (f) and decreased inspiratory (TI) and expiratory time (TE) in sleeping adult cats. We now hypothesized that almitrine would induce an increase in ventilation in a young animal model. Respiration was studied by the barometric method in 11 unanesthetized New Zealand White rabbit pups between 3 and 6 days of age. Recordings were made in 0.21 FIO2 at base line and after cumulative intraperitoneal infusions of almitrine (2.5, 5.0, and 7.5 mg/kg). The chamber pressure deflection (proportional to VT after appropriate calculation) was computer sampled at 200 Hz. At least 100 breaths for each dose in each animal were analyzed. We found that a 7.5-mg/kg intraperitoneal dose of almitrine increased f to 135 +/- 9% (SE) of base line and decreased TE and TI to 72 +/- 8% and 79 +/- 8% of base line, respectively. Changes in VE, VT/TI, and VT were not significant. Recognizing that apnea is associated with inadequate ventilation and a prolonged TE (failure of the "inspiratory on-switch"), these results, particularly the increase in f and decrease in TE, suggest that almitrine might be useful in treating apnea in preterm infants.     

Breathing patterns during submaximal and maximal exercise in elite oarsmen

Continuous breath-by-breath measurements of ventilatory parameters were performed during submaximal and maximal treadmill exercise in 21 highly conditioned oarsmen. Average maximum values of O2 uptake, minute ventilation (VI), tidal volume (VT), and respiratory frequency (f) were 6.60 l/min (73.5 ml X kg-1 X min-1), 200 l/min, 3.29 l, and 62 breaths/min, respectively. During the transition from moderate to heavy submaximal exercise, VT and f increased progressively. At near-maximal to maximal work loads, VT plateaued and then decreased slightly, while f continued to increase. Increase in f at the start of exercise was achieved predominantly by an abrupt decrease in expiratory duration (TE) with an equally abrupt, but much smaller, decrease in inspiratory duration (TI). During the transition from submaximal to maximal exercise, both TE and TI decreased progressively. Although f appeared to be entrained by stepping rate in a few subjects, the dominant trend during submaximal to maximal exercise was characterized by a relatively small increase in stepping rate with a much larger increment in f. Our data are consistent with the conclusion that exercise breathing patterns are determined by many interacting factors that vary at different work loads, in different individuals, and are probably also influenced by physical conditioning and previous experience.     

Breathing pattern in highly competitive cyclists during incremental exercise

The purpose of our investigation was to analyse the breathing patterns of professional cyclists during incremental exercise from submaximal to maximal intensities. A group of 11 elite amateur male road cyclists [E, mean age 23 (SD 2) years, peak oxygen uptake (VO2peak) 73.8 (SD 5.0) ml kg(-1) min(-1)] and 14 professional male road cyclists [P, mean age 26 (SD 2) years, (VO2peak) 73.2 (SD 6.6) ml kg(-1) min(-1)] participated in this study. Each of the subjects performed an exercise test on a cycle ergometer following a ramp protocol (exercise intensity increases of 25 W x min(-1)) until the subject was exhausted. For each subject, the following parameters were recorded during the tests: oxygen consumption (VO2), carbon dioxide output (VCO2), pulmonary ventilation (VE), tidal volume (VT), breathing frequency (fb), ventilatory equivalents for oxygen (VE x VO2(-1)) and carbon dioxide (VE x VCO2(-1)), end-tidal partial pressure of oxygen and partial pressure of carbon dioxide, inspiratory (tI) and expiratory (tE) times, inspiratory duty cycle (tI/tTOT, where tTOT is the time for one respiratory cycle), and mean inspiratory flow rate (VT/tI). Mean values of VE were significantly higher in E at 300, 350 and 400 W (P < 0.05, P < 0.05 and P < 0.01, respectively); fb was also higher in E in most moderate-to-maximal intensities. On the other hand, VT showed a different pattern in both groups at near-to maximal intensities, since no plateau was observed in P. The response of tI and tE was also different. Finally, VT/tI and tI/tTOT showed a similar response in both P and E. It was concluded that the breathing pattern of the two groups differed mainly in two aspects: in the professional cyclists, VE increased at any exercise intensity as a result of increases in both VT and fb, with no evidence of tachypnoeic shift, and tE was prolonged in this group at high exercise intensities. In contrast, neither the central drive nor the timing component of respiration seem to have been significantly altered by the training demands of professional cycling.     

Ventilatory response to high-frequency airway oscillation in humans

To investigate respiratory control during high-frequency oscillation (HFO), ventilation was monitored in conscious humans by respiratory inductive plethysmography during application at the mouth of high-frequency pressure oscillations. Studies were conducted before and after airway and pharyngeal anesthesia. During HFO, breathing became slow and deep with an increase in tidal volume (VT) of 37% (P less than 0.01) and inspiratory duration (TI) of 34% (P less than 0.01). Timing ratio (TI/TT) increased 14% (P less than 0.05) and respiratory frequency (f) decreased 12% (P less than 0.01). Mean inspiratory flow (VT/TI) did not change during HFO. Following airway anesthesia, VT increased only 26% during HFO (P less than 0.01), whereas significant changes in TI, TI/TT, and f were not observed. Pharyngeal anesthesia failed to diminish the effect of HFO on TI, TT, or f, although the increase in VT was reduced. These results indicate that 1) HFO presented in this manner alters inspiratory timing without affecting the level of inspiratory activity, and 2) receptors in the larynx and/or lower airways may in part mediate the response.     

Pattern of breathing in the rat.

The basic ventilation values - tidal volume (VT), breathing frequency (f), minute ventilation (VE) and the duration of inspiration (TI) and expiration (TE) -- were determined in adult male rats. The range of these values is given and the pattern of breathing is defined as the relationship between VE and VT, which in the rat is linear throughout its entire range. The role of TI and TE in changing f in the rat were evaluated. The breathing pattern of the rat was compared with data for the rabbit and man, using percentual expression of the basic values. A shift of the breathing pattern to higher f values was observed in rats with experimental lung diseases. In these rats, the inhalation of 100% O2 shifted the pattern of breathing markedly to lower VE values, though not to values comparable with the controls. Bilateral cervical vagotomy was followed by a pronouced decrease in f, an increase in VT and T1 persisted even after vagotomy, however; it can be assumed that this relationship is effected either by means of receptors in the chest muscles, or by the direct action of CO2 which is used to stimulate breathing, on the bulbopontine pacemaker.     

Effect of elastic loading on ventilatory pattern during progressive exercise

Ventilatory responses to progressive exercise, with and without an inspiratory elastic load (14.0 cmH2O/l), were measured in eight healthy subjects. Mean values for unloaded ventilatory responses were 24.41 +/- 1.35 (SE) l/l CO2 and 22.17 +/- 1.07 l/l O2 and for loaded responses were 24.15 +/- 1.93 l/l CO2 and 20.41 +/- 1.66 l/l O2 (P greater than 0.10, loaded vs. unloaded). At levels of exercise up to 80% of maximum O2 consumption (VO2max), minute ventilation (VE) during inspiratory elastic loading was associated with smaller tidal volume (mean change = 0.74 +/- 0.06 ml; P less than 0.05) and higher breathing frequency (mean increase = 10.2 +/- 0.98 breaths/min; P less than 0.05). At levels of exercise greater than 80% of VO2max and at exhaustion, VE was decreased significantly by the elastic load (P less than 0.05). Increases in respiratory rate at these levels of exercise were inadequate to maintain VE at control levels. The reduction in VE at exhaustion was accompanied by significant decreases in O2 consumption and CO2 production. The changes in ventilatory pattern during extrinsic elastic loading support the notion that, in patients with fibrotic lung disease, mechanical factors may play a role in determining ventilatory pattern.     

Effects of sleep-induced increases in upper airway resistance on ventilation

To determine the effects of the sleep-induced increases in upper airway resistance on ventilatory output, we studied five subjects who were habitual snorers but otherwise normal while awake (AW) and during non-rapid-eye-movement (NREM) sleep under the following conditions: 1) stage 2, low-resistance sleep (LRS); 2) stage 3-4, high-resistance sleep (HRS) (snoring); 3) with continuous positive airway pressure (CPAP); 4) CPAP + end-tidal CO2 partial pressure (PETCO2) mode isocapnic to LRS; and 5) CPAP + PETCO2 isocapnic to HRS. We measured ventilatory output via pneumotachograph in the nasal mask, PETCO2, esophageal pressure, inspiratory and expiratory resistance (RL,I and RL,E). Changes in PETCO2 were confirmed with PCO2 measurements in arterialized venous blood in all conditions in one subject. During wakefulness, pulmonary resistance (RL) remained constant throughout inspiration, whereas in stage 2 and especially in stage 3-4 NREM sleep, RL rose markedly throughout inspiration. Expired minute ventilation (VE) decreased by 12% in HRS, and PETCO2 increased in LRS (3.3 Torr) and HRS (4.9 Torr). CPAP decreased RL,I to AW levels and increased end-expiratory lung volume 0.25-0.93 liter. Tidal volume (VT) and mean inspiratory flow rate (VT/TI) increased significantly with CPAP. Inspiratory time (TI) shortened, and PETCO2 decreased 3.6 Torr but remained 1.3 Torr above AW. During CPAP (RL,I equal to AW), with PETCO2 returned to the level of LRS, VT/TI and VE were 83 and 52% higher than during LRS alone. Also on CPAP, with PETCO2 made equal to HRS, VT, VT/TI, and VE were 67, 112, and 67% higher than during HRS alone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of ozone on breathing in dogs: vagal and nonvagal mechanisms

We exposed two awake dogs with a chronic tracheostomy and the cervical vagus nerves exteriorized in skin loops to 1.0 ppm of ozone (O3) for 2 h at intervals of 4 wk. We measured ventilatory variables before and after O3 exposure during rest and exercise before and after vagal block. We compared the effects of vagal blockade, exercise, and O3 on the primary determinants of breathing pattern (VT/TI, VT/TE, TI, and TE) in each of three conditions: base line (steady state), during hypercapnia, and after inhalation of 1% histamine. Under base-line conditions, O3 increased respiratory rate and decreased tidal volume (VT) by shortening time of expiration (TE) and time of inspiration (TI) without affecting VT/TI, an indicator of the neural drive to breathing. During progressive hypercapnia, O3 shortened TE and TI by effects both on tonic (nonvolume-related) and on phasic (volume-related) vagal inputs, and only the latter were prevented completely by cooling of the vagus nerves. Histamine-induced tachypnea was increased by O3 and was totally blocked by cooling the vagus nerves. We conclude that O3 shortens the timing of respiration without increasing ventilatory drive, shortens TI and TE through vagal and nonvagal pathways, increases tonic nonvagal and phasic vagal inputs, and stimulates more than one vagal fiber type.     

Postnatal maturation of respiration in intact and carotid body-chemodenervated lambs

The contribution of the carotid body chemoreceptor to postnatal maturation of breathing was evaluated in lambs from 7 to 70 days of age. The study was conducted by comparing the eupneic ventilation and resting pneumograms in intact conscious lambs with those of lambs that were carotid body chemodenervated (CBD) at birth. In comparison to the 1-wk-old intact lambs, the CBD lambs had significant decreases in minute ventilation (VE, 313 vs. 517 ml/kg), tidal volume (VT, 7.2 vs. 10.5 ml/kg), respiratory rate (f, 44 vs. 51 breaths/min), and occlusion pressure (P0.1, 2.8 vs. 7.2 cmH2O). Arterial PO2's were 59 vs. 75 Torr (P less than 0.05) and arterial PCO2's 47 vs. 36 Torr (P less than 0.05), respectively, in CBD and intact lambs. In intact lambs from 7 to 70 days, resting VE decreased progressively from 517 to 274 ml/kg (P less than 0.01) due to a fall in VT, mean inspiratory flow (VT/TI), and f, whereas the ratio of inspiratory time to total breath duration remained constant. P0.1 decreased from 7.2 to 3.9 cmH2O from 7 to 42 days. In contrast the CBD lambs experienced only minimal changes in VE, VT, VT/TI, and f during the same period. VE only decreased from 313 to 218 and P0.1 from 2.8 to 2.4 cmH2O. In contrast to that of intact lambs the resting pneumogram of CBD lambs remained relatively fixed from 7 to 70 days. Three CBD lambs died unexpectedly, without apparent cause, in the 4th and 5th wk of life.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heart rate and breathing pattern: interactions and sex differences

Ten subjects (five males, five females) were studied in resting conditions. Ventilation (VT, f, TI, TE), heart rate (HR) and RR interval were recorded or measured. Each subject voluntarily breathed with spontaneous frequency at different ratios of his spontaneous tidal volume (VrT). The results show that sinus arrhythmia increases with lung volume but without effect on mean heart rate. When VT is increased by two times its spontaneous value, the ventilatory drive (VT/TI) is raised in both sexes; the relative duration of inspiration (TI/Ttot) is modified (+20%) in females only. Thus with the cardiac effects of increasing lung volume being similar in both sexes, we conclude that sinus arrhythmia is not generated by sensory inputs from pulmonary structures, but that its origin is at the CNS level. Moreover, there may be a sex difference in the control of voluntary ventilation, a suggestion requiring further investigation.     

Abolition of ventilatory response to caffeine in chemodenervated lambs

In this study we have evaluated the role of the peripheral chemoreceptors in the ventilatory response to caffeine at a dose currently used in human infants for treatment of central apneas (10 mg/kg). Twelve lambs were studied; six had carotid body denervation (CBD) and six had a sham denervation (intact). The denervation was done the 2nd wk of life, and the study of the response to caffeine infusion was carried out at a mean age of 82 days. The awake and nonsedated animals received 10 mg/kg of caffeine, and caffeine blood levels were, respectively, 8.8 and 9.0 mg/l in the intact and in the CBD lambs. The intact lambs responded to caffeine by a significant immediate increase in minute ventilation (VE) of 46% from 274 to 400 ml X min-1 X kg-1 (P less than 0.001), 1 min after caffeine infusion. This response rapidly faded, but VE was still increased at 2 h, 314 ml X min-1 X kg-1. The increase in ventilation was brought about by a change in mean inspiratory flow (VT/TI), which increased from 9.9 to 14.0 ml X s-1 X kg-1 within 1 min (P less than 0.01); VT/TI was still increased at 11.2 ml X s-1 X kg-1 2 h later. In contrast, for the CBD lambs there was no response to caffeine infusion as measured by VE or VT/TI. We conclude that bolus caffeine infusion produces a rapid response in VE followed by a fall in VE that remained above base line until at least 2 h postinfusion, and the intact chemoreceptor function appears as an essential mediator for these increases in ventilation, since the peripheral chemodenervation has completely abolished the VE response to this particular dose of caffeine.