Laryngeal and pump muscle activities during CO2 breathing in neonates

1993 ◽  
Vol 75 (1) ◽  
pp. 416-423 ◽  
Author(s):  
J. A. Wozniak ◽  
A. A. Hutchison ◽  
P. C. Kosch
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Quiet Sleep ◽  
Flow Rates ◽  
Co2 Gas ◽  
Posterior Cricoarytenoid ◽  
And Control ◽  
Expiratory Flow Rates

Term human newborns were challenged with a 2–3% CO2 gas mixture during quiet sleep. A common ventilatory response, consisting of increased tidal volume with no change in respiratory frequency or timing, was observed in all eight subjects. Minute ventilation and mean inspiratory and expiratory flow rates were elevated in all eight subjects [38 +/- 8 (SE), 38 +/- 22, and 39 +/- 9%, respectively]. Diaphragm, intercostal, and posterior cricoarytenoid (PCA) muscle activities during inspiration were increased in four of eight, six of eight, and seven of eight subjects, respectively Changes in intercostal and PCA muscle activities correlated with changes in inspiratory flow rates (r = 0.77 and 0.66, respectively). Diaphragmatic braking of expiratory airflow varied between subjects during room air breathing and did not change in six subjects with CO2 breathing. The remaining two subjects increased postinspiratory inspiratory diaphragmatic activity. Baseline expiratory PCA activity was augmented with CO2 breathing in six of eight subjects and correlated with increases in mean expiratory airflow (r = 0.76). The newborn infant is capable of using a variety of breathing strategies to augment tidal volume and minute ventilation, and control of the upper airway appears to be critical in modulating airflow during CO2 breathing.

Ventilatory response to hypoxia in unanesthetized newborn kittens

1988 ◽  
Vol 64 (6) ◽  
pp. 2544-2551 ◽  
Author(s):  
H. Rigatto ◽  
C. Wiebe ◽  
C. Rigatto ◽  
D. S. Lee ◽  
D. Cates
Keyword(s):  
Tidal Volume ◽  
Chest Wall ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Quiet Sleep ◽  
Newborn Kitten ◽  
Peripheral Mechanism ◽  
Flow Through ◽  
Ventilatory Response To Hypoxia

We studied the ventilatory response to hypoxia in 11 unanesthetized newborn kittens (n = 54) between 2 and 36 days of age by use of a flow-through system. During quiet sleep, with a decrease in inspired O2 fraction from 21 to 10%, minute ventilation increased from 0.828 +/- 0.029 to 1.166 +/- 0.047 l.min-1.kg-1 (P less than 0.001) and then decreased to 0.929 +/- 0.043 by 10 min of hypoxia. The late decrease in ventilation during hypoxia was related to a decrease in tidal volume (P less than 0.001). Respiratory frequency increased from 47 +/- 1 to 56 +/- 2 breaths/min, and integrated diaphragmatic activity increased from 14.9 +/- 0.9 to 20.2 +/- 1.4 arbitrary units; both remained elevated during hypoxia (P less than 0.001). Younger kittens (less than 10 days) had a greater decrease in ventilation than older kittens. These results suggest that the late decrease in ventilation during hypoxia in the newborn kitten is not central but is due to a peripheral mechanism located in the lungs or respiratory pump and affecting tidal volume primarily. We speculate that either pulmonary bronchoconstriction or mechanical uncoupling of diaphragm and chest wall may be involved.

Effect of Almitrine on Ventilation and on Diaphragm and Geniohyoid Muscle Activity in the Rat

1996 ◽  
Vol 91 (3) ◽  
pp. 337-345 ◽  
Author(s):  
Ken D. O'halloran ◽  
Aidan K. Curran ◽  
Aidan Bradford
Keyword(s):  
Tidal Volume ◽  
Muscle Activity ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Superior Laryngeal Nerve ◽  
Upper Airway ◽  
Laryngeal Nerve ◽  
Respiratory Frequency ◽  
Diaphragm Muscle ◽  
Arterial Blood

1. Ventilation was measured during normoxia, hypoxia and hypercapnia before and after administration of almitrine in conscious, unrestrained, tracheostomized rats with the superior laryngeal nerves intact or cut. In superior laryngeal nerve-intact animals breathing air, almitrine increased minute ventilation due to an increase in respiratory frequency with no change in tidal volume. In superior laryngeal nerve-sectioned animals, the minute ventilatory response to almitrine was reduced due to a reduced tidal volume component of the response. Almitrine increased the ventilatory response to hypercapnia in superior laryngeal nerve-intact but not in sectioned animals. 2. In anaesthetized, vagotomized rats breathing spontaneously through a low-cervical tracheostomy, diaphragm and geniohyoid electromyographic activities were recorded. Arterial blood pressure and rectal temperature were continuously monitored. A single dose of almitrine was administered intravenously. In all animals, the geniohyoid muscle had phasic inspiratory activity which slightly preceded diaphragm activity. Almitrine had no effect on respiratory frequency or inspiratory and expiratory duration but increased mean peak integrated diaphragm (+29.3 ±13.6%) and geniohyoid (+ 132.0 ±21.3%) muscle activity. 3. These results show that almitrine exerts part of its ventilatory effects through superior laryngeal nerve afferents. Almitrine preferentially excites upper airway compared with diaphragm muscle activity, suggesting a potential role in the alleviation of obstructive apnoea.

Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2

1988 ◽  
Vol 64 (5) ◽  
pp. 1885-1892 ◽  
Author(s):  
C. Shindoh ◽  
W. Hida ◽  
Y. Kikuchi ◽  
T. Chonan ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Co2 Response ◽  
Co2 Gas ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
And Control

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.

Decreased Carbon Dioxide Sensitivity in Infants of Substance-Abusing Mothers

PEDIATRICS ◽  
1995 ◽  
Vol 95 (6) ◽  
pp. 864-867
Author(s):  
Janet G. Wingkun ◽  
Janet S. Knisely ◽  
Sidney H. Schnoll ◽  
Gary R. Gutcher
Keyword(s):  
Carbon Dioxide ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Demographic Data ◽  
Substance Abusing ◽  
Quiet Sleep ◽  
Co2 Level ◽  
The Difference ◽  
End Tidal ◽  
Drug Free

Objective. To determine whether there is a demonstrable abnormality in control of breathing in infants of substance-abusing mothers during the first few days of life. Methods. We enrolled 12 drug-free control infants and 12 infants of substance abusing mothers (ISAMs). These infants experienced otherwise uncomplicated term pregnancies and deliveries. The infants were assigned to a group based on the results of maternal histories and maternal and infant urine toxicology screens. Studies were performed during quiet sleep during the first few days of life. We measured heart rate, oxygen saturations via a pulse oximeter, end-tidal carbon dioxide (ET-CO2) level, respiratory rate, tidal volume, and airflow. The chemoreceptor response was assessed by measuring minute ventilation and the ET-CO2 level after 5 minutes of breathing either room air or 4% carbon dioxide. Results. The gestational ages by obstetrical dating and examination of the infants were not different, although birth weights and birth lengths were lower in the group of ISAMs. Other demographic data were not different, and there were no differences in the infants' median ages at the time of study or in maternal use of tobacco and alcohol. The two groups had comparable baseline (room air) ET-CO2 levels, respiratory rates, tidal volumes, and minute ventilation. When compared with the group of ISAMs, the drug-free group had markedly increased tidal volume and minute ventilation on exposure to 4% carbon dioxide. These increases accounted for the difference in sensitivity to carbon dioxide, calculated as the change in minute ventilation per unit change in ET-CO2 (milliliters per kg/min per mm Hg). The sensitivity to carbon dioxide of control infants was 48.66 ± 7.14 (mean ± SE), whereas that of ISAMs was 16.28 ± 3.14. Conclusions. These data suggest that ISAMs are relatively insensitive to challenge by carbon dioxide during the first few days of life. We speculate that this reflects an impairment of the chemoreceptor response.

Response to Acute Hypercapnia in the Parents of Victims of Sudden Infant Death Syndrome

PEDIATRICS ◽  
1984 ◽  
Vol 73 (5) ◽  
pp. 652-655
Author(s):  
Jonathan M. Couriel ◽  
Anthony Olinsky
Keyword(s):  
Tidal Volume ◽  
Sudden Infant Death Syndrome ◽  
Infant Death ◽  
Cycle Time ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Sudden Infant Death ◽  
Respiratory Cycle ◽  
Sudden Infant ◽  
Inspiratory Time

The ventilatory response to acute hypercapnia was studied in 68 parents of victims of sudden infant death syndrome and 56 control subjects. Tidal volume, inspiratory time, and total respiratory cycle time were measured before and immediately after a vital capacity breath of 13% CO2 in oxygen. Instantaneous minute ventilation, mean inspiratory flow (tidal volume/inspiratory time), and respiratory timing (inspiratory time/total respiratory cycle time) were calculated. Both groups of subjects showed a marked increase in tidal volume (48.4% ± 26.5%), instantaneous minute ventilation (56% ± 35%), and tidal volume/inspiratory time (56.8% ± 33.5%) after inhalation of the test gas, with little change in inspiratory time/total respiratory cycle time. There were no significant differences between the two groups for ventilation before or after inhalation of the test gas. The ventilatory response to acute hypercapnia is mediated by the peripheral chemoreceptors. These results suggest that an inherited abnormality of peripheral chemoreceptor function is unlikely to be a factor leading to sudden infant death syndrome.

Tachykinins mediate bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs

1989 ◽  
Vol 66 (3) ◽  
pp. 1108-1112 ◽  
Author(s):  
D. W. Ray ◽  
C. Hernandez ◽  
A. R. Leff ◽  
J. M. Drazen ◽  
J. Solway
Keyword(s):  
Tidal Volume ◽  
Guinea Pigs ◽  
Minute Ventilation ◽  
Response Curves ◽  
Mechanically Ventilated ◽  
Stimulus Response ◽  
Respiratory System Resistance ◽  
Water Saturated ◽  
And Control ◽  
Isocapnic Hyperpnea

We tested the hypothesis that tachykinins mediate hyperpnea-induced bronchoconstriction (HIB) in 28 guinea pigs. Stimulus-response curves to increasing minute ventilation with dry gas were generated in animals depleted of tachykinins by capsaicin pretreatment and in animals pretreated with phosphoramidon, a neutral metalloendopeptidase inhibitor. Sixteen anesthetized guinea pigs received capsaicin (50 mg/kg sc) after aminophylline (10 mg/kg ip) and terbutaline (0.1 mg/kg sc). An additional 12 animals received saline (1 ml sc) instead of capsaicin. One week later, all animals were anesthetized, given propranolol (1 mg/kg iv), and mechanically ventilated (6 ml/kg, 60 breaths/min, 50% O2 in air fully water saturated). Phosphoramidon (0.5 mg iv) was administered to five of the noncapsaicin-treated guinea pigs. Eucapnic dry gas (95% O2–5% CO2) hyperpnea “challenges” were performed by increasing the tidal volume (2–6 ml) and frequency (150 breaths/min) for 5 min. Capsaicin-pretreated animals showed marked attenuation in HIB, with a rightward shift of the stimulus-response curve compared with controls; the estimated tidal volume required to elicit a twofold increase in respiratory system resistance (ES200) was 5.0 ml for capsaicin-pretreated animals vs. 3.7 ml for controls (P less than 0.03). Phosphoramidon-treated animals were more reactive to dry gas hyperpnea compared with control (ES200 = 2.6 ml; P less than 0.0001). Methacholine dose-response curves (10(-11) to 10(-7) mol iv) obtained at the conclusion of the experiments were similar among capsaicin, phosphoramidon, and control groups. These findings implicate tachykinin release as an important mechanism of HIB in guinea pigs.

Ventilatory response to exercise in diabetic subjects with autonomic neuropathy

1996 ◽  
Vol 81 (5) ◽  
pp. 1978-1986 ◽  
Author(s):  
C. Tantucci ◽  
P. Bottini ◽  
M. L. Dottorini ◽  
E. Puxeddu ◽  
G. Casucci ◽  
...  
Keyword(s):  
Respiratory Rate ◽  
Autonomic Neuropathy ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Control Subjects ◽  
Inhibitory Modulation ◽  
End Tidal ◽  
And Control ◽  
Response To Exercise ◽  
Maximal Voluntary Ventilation

Tantucci, C., P. Bottini, M. L. Dottorini, E. Puxeddu, G. Casucci, L. Scionti, and C. A. Sorbini. Ventilatory response to exercise in diabetic subjects with autonomic neuropathy. J. Appl. Physiol. 81(5): 1978–1986, 1996.—We have used diabetic autonomic neuropathy as a model of chronic pulmonary denervation to study the ventilatory response to incremental exercise in 20 diabetic subjects, 10 with (Dan+) and 10 without (Dan−) autonomic dysfunction, and in 10 normal control subjects. Although both Dan+ and Dan− subjects achieved lower O2 consumption and CO2 production (V˙co 2) than control subjects at peak of exercise, they attained similar values of either minute ventilation (V˙e) or adjusted ventilation (V˙e/maximal voluntary ventilation). The increment of respiratory rate with increasing adjusted ventilation was much higher in Dan+ than in Dan− and control subjects ( P < 0.05). The slope of the linearV˙e/V˙co 2relationship was 0.032 ± 0.002, 0.027 ± 0.001 ( P < 0.05), and 0.025 ± 0.001 ( P < 0.001) ml/min in Dan+, Dan−, and control subjects, respectively. Both neuromuscular and ventilatory outputs in relation to increasingV˙co 2 were progressively higher in Dan+ than in Dan− and control subjects. At peak of exercise, end-tidal [Formula: see text] was much lower in Dan+ (35.9 ± 1.6 Torr) than in Dan− (42.1 ± 1.7 Torr; P < 0.02) and control (42.1 ± 0.9 Torr; P < 0.005) subjects. We conclude that pulmonary autonomic denervation affects ventilatory response to stressful exercise by excessively increasing respiratory rate and alveolar ventilation. Reduced neural inhibitory modulation from sympathetic pulmonary afferents and/or increased chemosensitivity may be responsible for the higher inspiratory output.

Effects of inhaled oxygen (up to 40%) on periodic breathing and apnea in preterm infants

1992 ◽  
Vol 72 (1) ◽  
pp. 116-120 ◽  
Author(s):  
Z. Weintraub ◽  
R. Alvaro ◽  
K. Kwiatkowski ◽  
D. Cates ◽  
H. Rigatto
Keyword(s):  
Birth Weight ◽  
Tidal Volume ◽  
Preterm Infants ◽  
Gestational Age ◽  
Minute Ventilation ◽  
Periodic Breathing ◽  
Respiratory Pattern ◽  
Quiet Sleep ◽  
Flow Through ◽  
Transcutaneous Po2

To discover whether increases in inhaled O2 fraction (FIO2; up to 40%) decrease apnea via an increase in minute ventilation (VE) or a change in respiratory pattern, 15 preterm infants (birth weight 1,300 +/- 354 g, gestational age 29 +/- 2 wk, postnatal age 20 +/- 9 days) breathed 21, 25, 30, 35, and 40% O2 for 10 min in quiet sleep. A nosepiece and a flow-through system were used to measure ventilation. Alveolar PCO2, transcutaneous PO2, and sleep states were also assessed. All infants had periodic breathing with apneas greater than or equal to 3 s. With an increase in FIO2 breathing became more regular and apneas decreased (P less than 0.001). This regularization in breathing was not associated with significant changes in VE. However, the variability of VE, tidal volume, and expiratory and inspiratory times decreased significantly. The results indicate that the more regular breathing observed with small increases in FIO2 was not associated with significant changes in ventilation. The findings suggest that the increased oxygenation decreases apnea and periodicity in preterm infants, not via an increase in ventilation, but through a decrease in breath-to-breath variability of VE.

Hypercapnia increases expiratory braking in preterm infants

1993 ◽  
Vol 75 (6) ◽  
pp. 2665-2670 ◽  
Author(s):  
E. C. Eichenwald ◽  
R. A. Ungarelli ◽  
A. R. Stark
Keyword(s):  
Tidal Volume ◽  
Premature Infants ◽  
Lung Volume ◽  
Newborn Infants ◽  
Emg Activity ◽  
Quiet Sleep ◽  
Activity Peak ◽  
Posterior Cricoarytenoid ◽  
Respiratory Muscle Activity ◽  
Ventilatory Response To Co2

In contrast to adults, newborn infants breathe from an elevated end-expiratory lung volume, determined by the interaction of airflow retardation (braking) by the diaphragm and larynx, and expiratory duration. To determine the effect of hypercapnia on this strategy, we examined changes in respiratory muscle activity and the ventilatory response to CO2 breathing in eight premature infants 33–34 wk gestational age in the first 3 postnatal days. We recorded tidal volume, airflow, and electromyograms (EMG) of the laryngeal abductor [posterior cricoarytenoid (PCA)], which abducts the vocal cords, and diaphragm during behaviorally determined quiet sleep in room air and during steady-state inhalation of 2% CO2 in air. As expected, tidal volume increased (P < 0.0005) without a change in inspiratory duration with hypercapnia. Unexpectedly, in all subjects, expiratory duration was longer during CO2 inhalation (P < 0.001), accompanied by marked changes in expiratory flow patterns consistent with increased expiratory braking. Diaphragm post-inspiratory EMG activity increased with hypercapnia (P < 0.005) with no change in baseline diaphragm or PCA EMG activity. Peak inspiratory EMG activity of the diaphragm and PCA increased with CO2 (10 and 37%, respectively; P < 0.05). We conclude that the mechanisms used to elevate end-expiratory lung volume are enhanced during hypercapnia in premature infants. This breathing strategy may be important in maintaining gas exchange in infants with lung disease.

Respiration of conscious kittens in acute hypoxia and effect of almitrine bismesylate

1985 ◽  
Vol 59 (1) ◽  
pp. 18-23 ◽  
Author(s):  
H. B. McCooke ◽  
M. A. Hanson
Keyword(s):  
Ambient Temperature ◽  
Tidal Volume ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Acute Hypoxia ◽  
Second Phase ◽  
Biphasic Response ◽  
Almitrine Bismesylate ◽  
Peak Increase ◽  
Ventilatory Response To Hypoxia

Respiration was measured noninvasively in conscious kittens at an ambient temperature of 28–32 degrees C. Inspired O2 fraction (FIO2) was reduced abruptly from 0.21 to 0.12, 0.10, or 0.08 for 5 min on the day of birth and then on days 4, 7, 14, and 28. The ventilatory response to hypoxia was biphasic, as reported previously in anesthetized kittens, with minute ventilation (VE) increasing in the first minute and then falling towards control over the next 4 min. The fall in VE was due to a consistent fall in tidal volume, the changes in frequency during the second phase being more variable. The size of the first phase of the response increased up to 14 days, but the time at which the peak increase in VE occurred was not correlated with age. The degree of the secondary fall in VE was similar at each age and at each FIO2 studied. The degree of the biphasic response was significantly reduced after administration of almitrine (2 mg/kg ip) on days 1 and 4, but almitrine did not affect the response in older kittens.

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