Positive- and negative-pressure breathing in newborn rat before and after anesthesia

1984 ◽  
Vol 57 (5) ◽  
pp. 1454-1461 ◽  
Author(s):  
D. Marlot ◽  
J. P. Mortola

We have examined the effects of changes in functional residual capacity (FRC), determined by positive and negative body surface pressures, on the breathing pattern of intact newborn rats, before and after barbiturate anesthesia. With distending pressures (between 1 and 4 cmH2O) minute ventilation decreased mainly due to a prolongation of the expiratory time. This response was more marked after anesthesia and accompanied by a fall in tidal volume. The time of peak expiratory flow (TE'), an index of expiratory flow resistance, was not changed before anesthesia and only slightly decreased after anesthesia. With collapsing pressures between 1 and 2 cmH2O only small changes in breathing pattern occurred, whereas the TE' increased in all cases and the flow profile indicated a maintenance of lung volume during expiration. These data indicate that tonic vagal information is present in the newborn rat and is substantially enhanced after barbiturates. The result that changes in breathing pattern are not fully matched by the changes in TE' and expiratory flow profile may indicate that the receptors which control the respiratory pattern are not the same as those involved in the regulation of the expiratory flow. The pressure-volume curve of the respiratory system was similar before and after anesthesia, and the intercept was close to the zero pressure value, indicating that the FRC of the newborn rat, differently from the human baby, is not actively maintained above the resting volume of the system.

1987 ◽  
Vol 62 (6) ◽  
pp. 2220-2223 ◽  
Author(s):  
F. J. Cerny

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.


1982 ◽  
Vol 53 (5) ◽  
pp. 1071-1079 ◽  
Author(s):  
W. J. Lamm ◽  
J. R. Hildebrandt ◽  
J. Hildebrandt ◽  
Y. L. Lai

Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated.


1979 ◽  
Vol 46 (5) ◽  
pp. 867-871 ◽  
Author(s):  
A. Vinegar ◽  
E. E. Sinnett ◽  
D. E. Leith

Awake mice (22.6--32.6 g) were anesthetized intravenously during head-out body plethysmography. One minute after pentobarbital sodium anesthesia, tidal volume had fallen from 0.28 +/- 0.04 to 0.14 +/- 0.02 ml and frequency from 181 +/- 20 to 142 +/- 8. Functional residual capacity (FRC) decreased by 0.10 +/- 0.02 ml. Expiratory flow-volume curves were linear, highly repeatable, and submaximal over substantial portions of expiration in awake and anesthetized mice; and expiration was interrupted at substantial flows that abruptly fell to and crossed zero as inspiration interrupted relaxed expiration. FRC is maintained at a higher level in awake mice due to a higher tidal volume and frequency coupled with expiratory braking (persistent inspiratory muscle activity or increased glottal resistance). In anesthetized mice, the absence of braking, coupled with reductions in tidal volume and frequency and a prolonged expiratory period, leads to FRCs that approach relaxation volume (Vr). An equation in derived to express the difference between FRC and Vr in terms of the portion of tidal volume expired without braking, the slope of the linear portion of the expiratory flow-volume curve expressed as V/V, the time fraction of one respiratory cycle spent in unbraked expiration, and respiratory frequency.


1986 ◽  
Vol 60 (3) ◽  
pp. 1060-1066 ◽  
Author(s):  
R. G. Castile ◽  
O. F. Pedersen ◽  
J. M. Drazen ◽  
R. H. Ingram

The effect of carbachol-induced central bronchoconstriction on density dependence of maximal expiratory flow (MEF) was assessed in five dogs. MEFs were measured on air and an 80% He-20% O2 mixture before and after local application of carbachol to the trachea. Airway pressures were measured using a pitot-static probe, from which central airway areas were estimated. At lower concentrations of carbachol the flow-limiting site remained in the trachea over most of the vital capacity (VC), and tracheal area and compliance decreased in all five dogs. In four dogs, decreases in choke point area predominated and produced decreases in flows. In one dog the increase in airway “stiffness” apparently offset the fall in area to account for an increase in MEF. Density dependence measured as the ratio of MEF on HeO2 to MEF on air at 50% of VC increased in all five dogs. Increases in density dependence appeared to be related to increases in airway stiffness at the choke point rather than decreases in gas-related airway pressure differences. Lower concentrations produced a localized decrease in tracheal area and extended the plateau of the flow-volume curve to lower lung volumes. Higher concentrations caused further reductions in tracheal area and greater longitudinal extension of bronchoconstriction, resulting in upstream movement of the site of flow limitation at higher lung volumes. Density dependence increased if the flow-limiting sites remained in the trachea at mid-VC but fell if the flow-limiting site had moved upstream by that volume.


1985 ◽  
Vol 58 (2) ◽  
pp. 528-533 ◽  
Author(s):  
J. P. Mortola ◽  
D. Magnante ◽  
M. Saetta

The passive mechanical time constant (tau pass) of the respiratory system is relatively similar among newborn mammalian species, approximately 0.15–0.2 s. However, breathing rate (f) is higher in smaller species than larger species in order to accommodate the relatively larger metabolic demands. Since tidal volume per kilogram is an interspecies constant, in the fastest breathing species the short expiratory time should determine a substantial dynamic elevation of the functional residual capacity (FRC). We examined the possibility of a difference in expiratory time constant between dynamic and passive conditions by analyzing the expiratory flow pattern of nine newborn unanesthetized species during resting breathing. In most newborns the late portion of the expiratory flow-volume curve was linear, suggesting muscle relaxation. The slope of the curve, which represents the dynamic expiratory time constant of the respiratory system (tau exp), varied considerably among animals (from 0.1 to 0.7 s), being directly related to the inspiratory time and inversely proportional to f. In relatively slow-breathing newborns, such as infants and piglets, tau exp is longer than tau pass most likely due to an increase in the expiratory laryngeal resistance and FRC is substantially elevated. On the contrary, in the fastest breathing newborns (such as rats and mice) tau exp is similar or even less than tau pass, because at these high rates dynamic lung compliance is lower than its passive value and the dynamic elevation of FRC is small. In dynamic conditions, therefore, the product of tau exp and f is maintained within narrow limits.


1981 ◽  
Vol 61 (6) ◽  
pp. 781-784 ◽  
Author(s):  
J. Savoy ◽  
S. Dhingra ◽  
N. R. Anthonisen

1. in 10 patients with pulmonary fibrosis and in seven control subjects, we measured the pressure at the mouth 0.1 s after onset of an inspiration against occluded airway (P0.1), minute ventilation (VI), breathing frequency (fr), tidal volume (VT), inspiratory duration (Tl) and calculated the mean inspiratory flow (VT/Tl) and the fraction of the breath cycle devoted to inspiration (Tl/Ttot.). in the patients measurements were made at normal arterial oxygen saturations (Sao2), before and after lignocaine airway anaesthesia. 2. Efficacy of airway anaesthesia was tested by the cough response to citric acid inhalation. 3. in pulmonary fibrosis P0.1, f1 and VT/Tl were greater than in the control subjects, VT and Tl, were smaller and Tl/Ttot. and VI were not different. 4. Effective airway anaesthesia did not modify P0.1 and breathing pattern parameters observed in pulmonary fibrosis. 5. These results suggest that airway receptors do not contribute to a major extent to the control of breathing in pulmonary fibrosis.


1977 ◽  
Vol 42 (3) ◽  
pp. 413-419 ◽  
Author(s):  
N. A. Saunders ◽  
M. F. Betts ◽  
L. D. Pengelly ◽  
A. S. Rebuck

We measured lung mechanics in seven healthy males during acute isocapnic hypoxia (PAO2 = 40–50 Torr; PACO2 = 38–42 Torr). Hypoxia was accompanied by increases in total lung capacity (mean increase +/- SD; 0.40 +/- 0.24 liters; P less than 0.005) functional residual capacity (0.34 +/- 0.25 liters; P less than 0.01) and residual volume (0.56 +/- 0.44 liters; P less than 0.02) in all subjects. Specific conductance of the lung decreased during hypoxia (P less than 0.02). The static deflation pressure-volume curve of the lung was shifted upward during hypoxia in all subjects. Resting end-expiratory recoil pressure of the lung was slightly, but not significantly lower during hypoxtic expiratory lung compliance was greater during hypoxia (0.39 +/- 0.04 l/cmH2O) than control measurements (0.31 +/- 0.05 l/cmH2O; P less than 0.005). No change was noted in dynamic lung compliance. All changes in lung mechanics were reversed within three minutes of reoxygenation. We conclude that acute isocapnic hypoxia increases total lung capacity in man and suggest that this may be due to the effect of hypoxia on the airways and pulmonary circulation.


1979 ◽  
Vol 46 (5) ◽  
pp. 927-931 ◽  
Author(s):  
Y. L. Lai

Lung volumes and respiratory pressures were measured in anesthetized male hamsters weighing an average 117 g. In 16 supine animals functional residual capacity (FRC) determined by body plethysmograph was 1.12 +/- 0.23 (SD) ml (about 20% total lung capacity, TLC) slightly and significantly larger than the FRC measured by saline displacement, 1.01 +/- 0.15 ml. Similar results were found in six prone animals. Paralysis did not significantly alter supine FRC. Contrary to published reports, pleural pressure (Ppl) estimated from esophageal pressure was negative at FRC. The fact that lung volume decreased by 0.2 ml (about 4% TLC) when the chest was opened at FRC provided additional evidence of negative Ppl at FRC. No consistent changes in the lung pressure-volume curve were found after the chest was opened. Deflation chest wall compliance just above FRC was about twice lung compliance. The vital capacity and reserve volumes in this study agreed with values reported in the literature. However, absolute lung volumes (TLC, FRC, and residual volume) were lower by about 1.4 ml, possibly because of earlier overestimates of box FRC.


1983 ◽  
Vol 55 (2) ◽  
pp. 368-376 ◽  
Author(s):  
T. Y. Sullivan ◽  
P. L. Yu

Minute ventilation (VE) and breathing pattern during an abrupt increase in fractional CO2 were compared in 10 normal subjects before and after airway anesthesia. Subjects breathed 7% CO2-93% O2 for 5 min before and after inhaling aerosolized lidocaine. As a result of airway anesthesia, VE and tidal volume (VT) were greater during hypercapnia, but there was no effect on inspiratory time (TI). Therefore, airway anesthesia produced an increase in mean inspiratory flow (VT/TI) during hypercapnia. The increase in VT/TI was compatible with an increase in neuromuscular output. There was no effect of airway anesthesia on the inspiratory timing ratio or the shape and position of the curve relating VT and TI. We also compared airway resistance (Raw), thoracic gas volume, forced vital capacity, forced expired volume at 1s, and maximum midexpiratory flow rate before and after airway anesthesia. A small (0.18 cmH2O X l-1 X s) decrease in Raw occurred after airway anesthesia that did not correlate with the effect of airway anesthesia on VT/TI. We conclude that airway receptors accessible to airway anesthesia play a role in hypercapnic VE.


PEDIATRICS ◽  
1987 ◽  
Vol 80 (1) ◽  
pp. 79-84
Author(s):  
Ashok Joshi ◽  
Tilo Gerhardt ◽  
Patty Shandloff ◽  
Eduardo Bancalari

Anemia may increase the risk of tissue hypoxia in preterm infants. This could lead to respiratory center depression and an increased risk for apnea. Heart rate and breathing pattern were recorded in 30 preterm infants (gestational age 30.0 ± 2.3 weeks, postnatal age 46.6 ± 20.8 days, and weight 1,438 ± 266 g) before and after a transfusion of 10 mL/kg of packed RBCs. All infants were stable clinically, breathing room air, and free of prolonged apneic episodes. After transfusion, hematocrit levels increased from 27.0% ± 2.5% to 35.8% ± 4.7%. Heart rate decreased from 157.2 ± 13.6 beats per minute to 148.4 ± 13.9 beats per minute. There was no change in respiratory rate or BP. The duration of periodic breathing decreased significantly, as did the duration of the longest periodic breathing episode (P < .01). The number of respiratory pauses lasting 5 to 10 seconds and the number of pauses lasting 11 to 20 seconds also decreased significantly (P < .05). The total duration of respiratory pauses, excluding pauses during periodic breathing, were significantly lower after transfusion (P < .05), as was the number of episodes of bradycardia. These results indicate that preterm infants have a more irregular breathing pattern while anemic than after correction of the anemia. The irregular breathing pattern is probably caused by mild hypoxic respiratory center depression.


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