Effect of frequency on perceived magnitude of added loads to breathing

Using open-magnitude scaling, six normal subjects estimated the perceived magnitude of a range of added elastic loads (20-76 cmH2O/l), applied for a sequence of five breaths, at frequencies varying from 5 to 26.4 breaths/min. Two experiments were performed. In the first, frequency was increased by a reduction in expiratory duration (TE), and the duty cycle (ratio of inspiratory duration to total breath duration, TI/TT) ranged between 0.10 and 0.52. The perceived magnitude psi increased significantly with the peak airway pressure (Pm) (P less than 0.0001) but did not reach conventional significance with frequency (fb) (P = 0.15): psi = K0Pm1.23fb0.07 (r = 0.911). However, the sensory magnitude increased significantly as the duty cycle increased (P less than 0.01), but when it was included, the magnitude decreased minimally with frequency (P less than 0.01): psi = K0Pm1.3fb-0.97 TI/TT1.14 (r = 0.92). In the second experiment the duty cycle (TI/TT) was kept constant [(0.43 +/- 0.008 (SE)] and frequency (5-26.4 breaths/min) increased at the expense of shortening both TI and TE. The perceived magnitude of the added elastances decreased with the increase in frequency. However, when the perceived magnitude was corrected for the duration of inspiration, which is known to increase the sensory magnitude, psi = K0Pm1.3TI0.56, the sensory magnitude increased significantly with frequency (P less than 0.001): psi/TI0.56 = K0Pm1.21fb0.28 (r = 0.773). The decrease in inspiratory duration had a greater quantitative effect decreasing sensory magnitude than frequency had on increasing the magnitude. The effect of increasing frequency is complex and depends on the simultaneous intensity, duration of inspiratory pressure, and the duty cycle.     

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.     

Power spectral density of breathing pattern in patients with chronic obstructive lung disease

Newsom Davis and Stagg studying the interrelationship of the volume and time components of individual breaths in healthy resting man described a significant correlation between mean tidal volume (VT) and inspiratory time (TI) r = 0.704. The correlation between mean TI and expiratory time (TE) was lower, r = 0.381. Evaluation of these relationships and of the power spectral density of the breathing pattern was the aim of the present study. For breath by breath analysis we calculated power spectral density and cross correlations of VT, TI and TE. We found a significant correlation between VT and TI in 9 patients with global respiratory insufficiency (RI) (mean r = 0.52) and 7 patients with partial RI (mean r = 0.56). The correlation between TI, TE was lower, in 9 patients with global RI (mean r = 0.21) and 7 patients with partial RI (mean r = 0.35). The results of both groups did not differ from healthy subjects in power spectral density of the breathing pattern and in correlations of VT and TI as well as TI and TE.     

Breath-by-breath interactions between inspiratory and expiratory duration in occlusive sleep apnea

We examined interactions between inspiratory duration (TI), expiratory duration (TE), and inspiratory (esophageal) pressure (Pes) generation in seven subjects with confirmed occlusive sleep apnea. Breath-by-breath values of TI, TE, and Pes were identified by digital computer during 21 260-s epochs of repetitive occlusive apnea during non-rapid-eye-movement sleep. The control theory of interacting nonlinear oscillators was used to categorize the interaction between TI and TE for each epoch as either 1) synchronization, the strongest possible interaction between biological oscillators; 2) relative entrainment, a moderate interaction between oscillators; or 3) relative coordination, a weak interaction. The latter two interactions were characterized by systemic oscillations in the moving cross-correlation between TI and TE. The relationship between TI and Pes was analyzed in a similar fashion. Significant oscillations were present in all three parameters (P less than 0.0001 for each). We observed significant negative correlations between TI and TE and between TI and Pes (P less than 0.001 for each) when all breaths for all epochs were pooled. In no epoch was there a significant positive correlation between TI and TE or Pes. All three interactions were observed between TI and TE: five epochs of synchronization, nine of relative entrainment, and seven of relative coordination. In contrast, 19 of 21 epochs exhibited synchronization between TI and Pes, with 2 epochs of relative entrainment. The relative frequency of TI vs. Pes synchronization was significantly greater than TI vs. TE synchronization (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Control of respiratory pattern in conscious dog: effects of heat and CO2

We measured tidal volume (VT) and inspiratory (TI) and expiratory (TE) durations in five conscious tracheostomized dogs breathing air or 5% CO2 in air either at normal (20 degrees C) or elevated (30 degrees C) ambient temperatures. Respiratory frequency ranged between 16 and 333/min due to changes in both TI and TE. During panting TI exceeded TE. During air inhalation instantaneous ventilation (V) spontaneously ranged from 100 to 1,600 ml . kg-1 . min-1. Hypercapnia, heat stress, or both, increased this range of V by increasing maximum V, primarily due to increases in mean inspiratory flow. Under these conditions, changes in TI accounted for more of the spontaneous changes in breath duration. During inhalation of air and 5% CO2, a positive correlation between VT and TI was obtained for TI between 0.13 and 1.05 s; above 1.05 s VT decreased. Heat stress increased VT at a given TI. We suggest that either the decay rate or position of the inspiratory off-switch threshold curve (Clark and von Euler, J. Physiol. London 222: 267, 1972) varies in conscious dogs. Shifts in either the reset (onset) value or decay rate of the curve yield a positive correlation between VT and TI. This modification to the Clark-von Euler model implies that the primary effect of anesthesia on respiratory control is fixation of the inspiratory off-switch threshold curve.     

Factors affecting tissue volume measurements in normal and edematous dog lungs

To characterize further some of the factors affecting lung tissue soluble-gas rebreathing volume (Vlt), we determined the solubility of acetylene in blood and lung tissue, the influence of the presence of pulmonary edema on tissue solubility, the effects of varying tidal volume (VT), and the tissue volume actually measured in two groups of six anesthetized paralyzed dogs: controls (C) and oleic acid-induced pulmonary edema (OA). Each animal's solubility was used to compute Vlt for comparison with gravimetric lung weight (Ql) and extravascular lung water content (Qwl). Solubility at 37.5 degrees C in blood (0.125 ml X 100 ml-1 X Torr-1) exceeded that in lung tissue (P less than 0.005): C = 0.118 and OA = 0.112 ml X 100 ml-1 X Torr-1 (NS). Vlt, expressed as %Ql, increased with increasing VT (20, 35, and 50 ml/kg) in OA (62.2, 78.9, and 94.7%, respectively, P less than 0.0001) but not in C (92.4, 94.4, and 99.3%, respectively). We conclude that solubility differs in blood and lung tissue but not in normal and edematous lungs, Vlt is not affected by VT in normal dogs but is in those with pulmonary edema, and Vlt measures Ql rather than Qwl.     

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.     

Respiratory timing during NREM sleep in patients with occlusive sleep apnea

To study respiratory timing mechanisms in patients with occlusive apnea, inspiratory and expiratory times (TI and TE) were calculated from the diaphragmatic electromyogram obtained in seven patients during non-rapid-eye-movement (NREM) sleep. Peak diaphragmatic activity (EMGdi) had a curvilinear relationship with TI during the ventilatory and occlusive phases such that TI shortened as EMGdi decreased during the ventilatory phase (r = 0.87, P less than 0.05) and it prolonged as EMGdi increased during the occlusive phase (r = 0.89, P less than 0.02). However, EMGdi vs. TI for the occlusive phase was shifted to the right of that for the ventilatory phase, reflecting the relatively longer TI during upper airway occlusion. TI also had a linear relationship with pleural pressure (r = 0.94, P less than 0.001) that remained unchanged during the ventilatory and occlusive phases such that it prolonged as negative inspiratory pressure increased. These results indicate that respiratory timing is continuously modified in patients with occlusive apnea as inspiratory neural drive fluctuates during NREM sleep and suggest that this modification is due to the net effects of changing inspiratory neural drive and afferent input predominantly from upper airway mechanoreceptors.     

On the relation between expiratory duration and subsequent inspiratory duration

To characterize respiratory interphase relationships in dogs, inspiratory duration (TI) or expiratory duration (TE) was systematically altered by electrical activation of vagal afferents, and the effect on subsequent TE or TI values was measured from the phrenic discharge. A linear TI-subsequent TE relationship was found. Following a vagally mediated prolongation of TE, 1) TI was prolonged, and the TE-subsequent TI relationship was curvilinear, 2) the threshold for inspiratory termination by phasic vagal inputs was increased, 3) the amplitude of the time course of the phrenic discharge was reduced so that the peak discharge reached the same level at inspiratory termination independent of TI, 4) the effect on TI prolongation persisted for several breaths whereas the effect was minimal on subsequent TE values, and 5) for tonic inputs the direct shortening of TI was nearly offset by the indirect lengthening of TI. These studies suggest the existence of slow central mechanisms that provide adaptation to elevated levels of vagal input in the control of TI. These mechanisms may also be responsible for the interphase timing relationships.     

Impedance electrodes positioned on proximal portions of limbs quantify fluid compartments in dogs

Body resistance and reactance to the conduction of an alternating electrical current were measured using electrodes attached to distal and proximal portions of limbs in anesthetized dogs. Body impedance was calculated from these measurements obtained at 30-min time intervals during a control period and after intravenous administration of 0.9% saline. Extracellular (ECW) and total body water (TBW) were determined by bromide and heavy water dilution techniques, respectively. Baseline impedance obtained from proximal electrodes was related to ECW (r = 0.95, P less than 0.001) and TBW (r = 0.80, P less than 0.02). After saline infusion, proximal electrodes detected a significant fall in impedance (P less than 0.001), whereas distal electrodes did not (P = 0.06). Furthermore, ECW and TBW could be estimated from the drop of proximal impedance after this bolus infusion (r = 0.82, P less than 0.02, and r = 0.86, P less than 0.01, respectively), but not from distal impedance measurements. Proximally placed impedance electrodes are superior to traditionally used distal electrodes for assessment of body fluid changes in the dog.     

Breathing pattern during exercise in young black and Caucasian subjects

Lung volumes in sex-, age-, height-, and weight-matched Black subjects are 10-15% lower than those in Caucasians. To determine whether this decreased lung volume affected the ventilatory adaptation to exercise, minute ventilation (VE), its components, frequency (f) and tidal volume (VT), and breathing pattern were observed during incremental cycle-ergometer exercise. Eighteen Caucasian (age 8-30 yr) and 14 Black (age 8-25 yr) subjects were studied. Vital capacity (VC) was lower (P less than 0.001) in the Black subjects [90.6 +/- 8.6 (SD) vs. 112.9 +/- 9.9% predicted], whereas functional residual capacity/total lung capacity was higher (P less than 0.05). VE, mixed expired O2 and CO2, VT, f, and inspiratory (TI), expiratory (TE), and total respiratory cycle (TT) duration were measured during the last 30 s of each 2-min load. Statistical comparisons with increasing power output were made at rest and from 0.6 to 2.4 W/kg in 0.3-W/kg increments. VE was higher in Blacks at all work loads and reached significance (P less than 0.05) at 0.6 and 1.5 W/kg. VE/VO2 was also higher throughout exercise, reaching significance (P less than 0.01) at 1.2, 1.5, and 1.8 W/kg. The Black subjects attained any given level of VE with a higher f (P less than 0.001) and lower VT. TI and TE were shortened proportionately so that TI/TT was not different. Differences in lung volume and the ventilatory response to exercise in these Black and Caucasian subjects suggest differences in the respiratory pressure-volume relationships or that the Black subjects may breathe higher on their pressure-volume curve.     

Role of the carotid chemoreceptors in regulation of inspiratory onset

We studied the effect of intermittent tidal breaths of CO2-enriched air (3-9% CO2) on the duration of expiratory time (TE) in five trained dogs, before and after (3 dogs) bilateral surgical denervation of the carotid bodies (CBD). During studies the dogs lay quietly, either awake or in nonrapid-eye-movement sleep, and breathed through a cuffed endotracheal tube inserted via a chronic tracheostomy. Studies were conducted during bilateral blockade of the cervical vagus nerves (VB), achieved by circulating cold alcohol through radiators placed around exteriorized vagal skin loops. Prior to CBD, single breaths of CO2 significantly shortened TE and thus advanced the onset of the subsequent inspiration. Further, the decrease in TE induced by the CO2 stimulus was in direct proportion to the inspired CO2 concentration. Thus 3% CO2 shortened TE by 1.82 +/- 0.93 (SD) s, and 9% CO2 by 3.44 +/- 1.53 s. Changes in TE occurred in the absence of associated changes in either tidal volume or inspiratory time. After CBD, test breaths of CO2 failed to shorten TE during VB. We conclude that the carotid bodies have the ability to mediate changes in the timing of inspiratory onset in response to a transient CO2 stimulus.     

Differential timing of respiratory muscles in response to chemical stimuli in awake dogs

We assessed changes in respiratory muscle timing in response to hyperpnea and shortened inspiratory and expiratory times caused by chemoreceptor stimuli in six awake dogs. Durations of postinspiratory inspiratory activity of costal and crural diaphragm (PIIA), the delay in diaphragm electromyogram (EMG) after the initiation of inspiratory airflow, postexpiratory expiratory activity of the transversus abdominis (PEEA), and the delay of abdominal expiratory muscle activity after the initiation of expiratory airflow were measured. In control, four out of six dogs showed PIIA [8-10% of expiratory time (TE)]; all showed delay of diaphragm [19% of inspiratory time (TI)], delay of abdominal muscle activation (21% of TE), and PEEA (24% of TI). Hypercapnia decreased PIIA (4-9% of TE), maintained diaphragm delay at near control values (23% of TI), increased PEEA (36% of TI), eliminated delay of abdominal muscle activation (4% of TE), and decreased end-expiratory lung volume (EELV). Hypocapnic hypoxia increased PIIA (24-25% of TE), eliminated diaphragm delay (3% of TI), eliminated PEEA (3% of TI), reduced delay of abdominal muscle activation (14% of TE), and increased EELV. Most of these effects of hypoxic hypocapnia vs. hypercapnia on the within-breath EMG timing parameters corresponded to differences in the magnitude of expiratory muscle activation. These changes exerted significant influences on flow rates and EELV.     

Phase resetting of the respiratory cycle before and after unilateral pontine lesion in cat.

The pontine respiratory group (PRG) facilitates the mechanism for terminating the inspiratory phase but may influence other phases in the respiratory cycle as well. We determined the effects of PRG lesions on the response of the respiratory cycle to superior laryngeal nerve stimulation delivered in each phase of the cycle in decerebrate, vagotomized, paralyzed, and ventilated cats (n = 6). We measured the duration of inspiration (TI) and expiration (TE) for three breaths before and in the perturbed breath and TI for three breaths after the perturbation. The delay to next inspiration was plotted against the phase at which the stimulus was delivered. Before lesioning, premature inspiratory termination was followed by phase-dependent shortening of TE. After lesioning, premature inspiratory termination did not systematically change the following TE. Breath-by-breath variability (measured 50 breaths) increased and stimulus after-effects (prolonged TI in the subsequent cycle) were augmented following lesions. These data indicate that the PRG plays an important role in the control of TE after perturbation and in the stability of the respiratory central pattern generator.     

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.     

Respiratory muscle oxygen consumption estimated by the diaphragm pressure-time index

The O2 consumption of the respiratory muscles (VO2resp), work of breathing, and the time integral of the transdiaphragmatic pressure (TTdi) were measured in four normal subjects breathing against inspiratory resistance. A total of 39 runs were performed at mean tidal transdiaphragmatic pressures (Pdi) ranging from 15 to 53 cmH2O, respiratory frequencies from 3.5 to 22 breaths/min, and inspiratory time durations (TI) from 32 to 76% of the total breath duration. Each run was maintained from 8 to 17 min and the above parameters were kept constant by the subject via visual feedback of Pdi and TI with an oscilloscope. Most of the runs (36 of 39) were performed at TTdi values below those known to produce respiratory muscle fatigue. We found a strong linear correlation between the VO2resp and the TTdi (r = 0.74, P less than 0.001) and a weaker correlation between VO2resp and W (r = 0.31, P less than 0.05). These data suggest that TTdi is a good estimator of VO2resp over a wide range of respiratory patterns during inspiratory resistance breathing. The high variability seen in respiratory muscle efficiency during resistive breathing may be due to W not being a good indicator of the energy consumed by the respiratory muscles.     

Effects of Vasopressin on Blood-Brain Transfer of Methionine in Dogs

We used a simplified probe detection system for positron-emitting radionuclides in order to measure blood-brain barrier transport of amino acids in anesthetized dogs. Plasma and brain time-activity curves were recorded after intravenous bolus injection of L-[11C]methionine before and after administration of 1 microgram of vasopressin. Three-compartment models with three or four transfer coefficients were used to derive the kinetics of L-[11C]methionine uptake in brain. The blood-brain clearance of the tracer (K1) was 0.075 ml ml-1 min-1 before and 0.041 ml ml-1 min-1 after injection of vasopressin. The partition volume and the initial distribution (plasma) volume of methionine were unchanged and within the expected limits. The net accumulation rate of methionine (K), estimated by both the four-parameter (kinetic) and three-parameter (graphic) approaches, decreased after vasopressin injection in all six studies.     

Central CO-heme oxygenase pathway raises body temperature by a prostaglandin-independent way.

Recently, the carbon monoxide (CO)-heme oxygenase pathway has been shown to play an important role in fever generation by acting on the central nervous system, but the mechanisms involved have not been assessed. Thus the present study was designed to determine whether prostagandins participate in the rise in body temperature (T(b)) observed after induction of the CO-heme oxygenase pathway in the central nervous system. Intracerebroventricular (ICV) injection of heme-lysinate (152 nmol/4 microl), which is known to induce the CO-heme oxygenase pathway, caused an increase in T(b) [thermal index (TI) = 5.3 +/- 0.5 degrees C. h], which was attenuated by ICV administration of the heme oxygenase inhibitor ZnDPBG (200 nmol/4 microl; TI = 2.5 +/- 1.7 degrees C. h; P < 0.05). No change in T(b) was observed after intraperitoneal injection of the cyclooxygenase inhibitor indomethacin (5 mg/kg), whereas indomethacin at the same dose attenuated the fever induced by ICV administration of lipopolysaccharide (LPS) (10 ng/2 microl) (vehicle/LPS: TI = 4.5 +/- 0.5 degrees C. h; indomethacin/LPS: TI = 1.7 +/- 1.0 degrees C. h; P < 0.05). Interestingly, indomethacin did not affect the rise in T(b) induced by heme-lysinate (152 nmol/4 microl) ICV injection (vehicle/heme: TI = 4.5 +/- 1.4 degrees C. h; indomethacin/heme: TI = 4.2 +/- 1.0 degrees C. h). Finally, PGE(2) (200 ng/2 microl) injected ICV evoked a rise in T(b) that lasted 1.5 h. The heme oxygenase inhibitor ZnDPBG (200 nmol/4 microl) failed to alter PGE(2)-induced fever. Taken together, these results indicate that the central CO-heme oxygenase pathway increases T(b) independently of prostaglandins.     

Nonrandom variability in respiratory cycle parameters of humans during stage 2 sleep

We analyzed breath-to-breath inspiratory time (TI), expiratory time (TE), inspiratory volume (VI), and minute ventilation (Vm) from 11 normal subjects during stage 2 sleep. The analysis consisted of 1) fitting first- and second-order autoregressive models (AR1 and AR2) and 2) obtaining the power spectra of the data by fast-Fourier transform. For the AR2 model, the only coefficients that were statistically different from zero were the average alpha 1 (a1) for TI, VI, and Vm (a1 = 0.19, 0.29, and 0.15, respectively). However, the power spectra of all parameters often exhibited peaks at low frequency (less than 0.2 cycles/breath) and/or at high frequency (greater than 0.2 cycles/breath), indicative of periodic oscillations. After accounting for the corrupting effects of added oscillations on the a1 estimates, we conclude that 1) breath-to-breath fluctuations of VI, and to a lesser extent TI and Vm, exhibit a first-order autoregressive structure such that fluctuations of each breath are positively correlated with those of immediately preceding breaths and 2) the correlated components of variability in TE are mostly due to discrete high- and/or low-frequency oscillations with no underlying autoregressive structure. We propose that the autoregressive structure of VI, TI, and Vm during spontaneous breathing in stage 2 sleep may reflect either a central neural mechanism or the effects of noise in respiratory chemical feedback loops; the presence of low-frequency oscillations, seen more often in Vm, suggests possible instability in the chemical feedback loops. Mechanisms of high-frequency periodicities, seen more often in TE, are unknown.     

Effects of focal cooling of medulla oblongata structures on quiet breathing in cats

Experiments were carried out on 16 anaesthetized, non-paralysed cats to determine the effects of unilateral, successive focal cooling of the nuclei of the dorsal and ventral respiratory groups (DRG, VRG) of the medulla oblongata on quiet breathing parameters. The results of cold block tests of the respiratory nuclei showed that: 1. Compared with the control state, cooling of the ventrolateral part of the nucleus solitarii (vl. NTS) and the rostral part of the nucleus retroambigualis (r. NRA) to 20 degrees C or 15 degrees C decreased the respiration rate (p less than 0.001), prolonged the inspiration time (p less than 0.01 and p less than 0.001 respectively) and the development of apneustic breathing. A decrease in the inspiratory pleural pressure values (p less than 0.01) was found after cooling the r. NRA region to 15 degrees C. In 45% of the cases of cooling of the vl. NTS and 66.7% of cooling of the r. NRA to 15 degrees C, an incidence of short inspiratory efforts was observed. 2. Focal cooling of the nucleus retrofacialis (nucl. RF) region to 20 degrees C always arrested rhythmic respiration. 3. The effects of unilateral focal cooling of the respiratory nuclei were always bilaterally symmetrical and, after discontinuing cooling, reversible. 4. The findings indicate that the inspiratory neurones of the r. NRA participate more in regulation of the intensity of inspiration than those of the vl. NTS, while the nucl. RF region may be a part of central regulatory mechanisms essential for the maintenance of rhythmic breathing in cats.