scholarly journals Volatile anesthetics maintain tidal volume and minute ventilation to a greater degree than propofol under spontaneous respiration

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Xuechao Hao ◽  
Mengchan Ou ◽  
Yu Li ◽  
Cheng Zhou
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Volatile Anesthetics ◽  
Whole Body ◽  
Spontaneous Respiration ◽  
General Anesthetics ◽  
Expiratory Time ◽  
Inhalational Anesthetics ◽  
Respiratory Parameters

Abstract Background Although general anesthetics depress spontaneous respiration, the comprehensive effect of general anesthetics on respiratory function remains unclear. We aimed to investigate the effects of general anesthetics on spontaneous respiration in non-intubated mice with different types and doses of general anesthetic. Methods Adult C57BL/6 J mice were administered intravenous anesthetics, including propofol and etomidate, and inhalational anesthetics, including sevoflurane and isoflurane in vivo at doses of 0.5-, 1.0-, and 2.0-times the minimum alveolar concentration (MAC)/median effective dose (ED50) to induce loss of the righting reflex (LORR). Whole-body plethysmography (WBP) was applied to measure parameters of respiration under unrestricted conditions without endotracheal intubation. The alteration in respiratory sensitivity to carbon dioxide (CO2) under general anesthesia was also determined. The following respiratory parameters were continuously recorded during anesthesia or CO2 exposure: respiratory frequency (FR), tidal volume (TV), minute ventilation (MV), expiratory time (TE), inspiratory time (TI), and inspiratory–expiratory time ratio (I/E), and peak inspiratory flow. Results Sub-anesthetic concentrations (0.5 MAC) of sevoflurane or isoflurane increased FR, TV, and MV. With isoflurane and sevoflurane exposure, the CO2-evoked increases in FR, TV, and MV were decreased. Compared with inhalational anesthetics, propofol and etomidate induced respiratory suppression, affecting FR, TV, and MV. In 100% oxygen (O2), FR in the group that received propofol 1.0-times the ED50 was 69.63 ± 33.44 breaths/min compared with 155.68 ± 64.42 breaths/min in the etomidate-treated group. In the same groups, FR was 88.72 ± 34.51 breaths/min and 225.10 ± 59.82 breaths/min, respectively, in 3% CO2 and 144.17 ± 63.25 breaths/min and 197.70 ± 41.93 breaths/min, respectively, in 5% CO2. A higher CO2 sensitivity was found in etomidate-treated mice compared with propofol-treated mice. In addition, propofol induced a greater decrease in FR, MV, and I/E ratio compared with etomidate, sevoflurane, and isoflurane at equivalent doses (all P < 0.05). Conclusions General anesthetics differentially modulate spontaneous breathing in vivo. Volatile anesthetics increase FR, TV, and MV at sub-anesthetic concentrations, while they decrease FR at higher concentrations. Propofol consistently depressed respiratory parameters to a greater degree than etomidate.

scholarly journals Regulation of breathing pattern by IL-10

2019 ◽  
Vol 317 (1) ◽  
pp. R190-R202 ◽  
Author(s):  
Charoula Eleni Giannakopoulou ◽  
Adamantia Sotiriou ◽  
Maria Dettoraki ◽  
Michael Yang ◽  
Fotis Perlikos ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Control Of Breathing ◽  
Neonatal Rat ◽  
Whole Body ◽  
Wild Type ◽  
Rapid Shallow Breathing Index ◽  
Regulation Of Breathing ◽  
Shallow Breathing

Proinflammatory cytokines like interleukin-1β (IL-1β) affect the control of breathing. Our aim is to determine the effect of the anti-inflammatory cytokine IL-10 οn the control of breathing. IL-10 knockout mice (IL-10−/−, n = 10) and wild-type mice (IL-10+/+, n = 10) were exposed to the following test gases: hyperoxic hypercapnia 7% CO2-93% O2, normoxic hypercapnia 7% CO2-21% O2, hypoxic hypercapnia 7% CO2-10% O2, and hypoxic normocapnia 3% CO2-10% O2. The ventilatory function was assessed using whole body plethysmography. Recombinant mouse IL-10 (rIL-10; 10 μg/kg) was administered intraperitoneally to wild-type mice ( n = 10) 30 min before the onset of gas challenge. IL-10 was administered in neonatal medullary slices (10–30 ng/ml, n = 8). We found that IL-10−/−mice exhibited consistently increased frequency and reduced tidal volume compared with IL-10+/+mice during room air breathing and in all test gases (by 23.62 to 33.2%, P < 0.05 and −36.23 to −41.69%, P < 0.05, respectively). In all inspired gases, the minute ventilation of IL-10−/−mice was lower than IL-10+/+(by −15.67 to −22.74%, P < 0.05). The rapid shallow breathing index was higher in IL-10−/−mice compared with IL-10+/+mice in all inspired gases (by 50.25 to 57.5%, P < 0.05). The intraperitoneal injection of rIL-10 caused reduction of the respiratory rate and augmentation of the tidal volume in room air and also in all inspired gases (by −12.22 to −29.53 and 32.18 to 45.11%, P < 0.05, respectively). IL-10 administration in neonatal rat ( n = 8) in vitro rhythmically active medullary slice preparations did not affect either rhythmicity or peak amplitude of hypoglossal nerve discharge. In conclusion, IL-10 may induce a slower and deeper pattern of breathing.

scholarly journals Ventilatory responses during and following hypercapnic gas challenge are impaired in male but not female endothelial NOS knock-out mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Paulina M. Getsy ◽  
Sripriya Sundararajan ◽  
Walter J. May ◽  
Graham C. von Schill ◽  
Dylan K. McLaughlin ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Whole Body ◽  
Inspiratory Time ◽  
Male And Female ◽  
Knock Out ◽  
Ventilatory Responses ◽  
Knock Out Mice ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

AbstractThe roles of endothelial nitric oxide synthase (eNOS) in the ventilatory responses during and after a hypercapnic gas challenge (HCC, 5% CO2, 21% O2, 74% N2) were assessed in freely-moving female and male wild-type (WT) C57BL6 mice and eNOS knock-out (eNOS-/-) mice of C57BL6 background using whole body plethysmography. HCC elicited an array of ventilatory responses that were similar in male and female WT mice, such as increases in breathing frequency (with falls in inspiratory and expiratory times), and increases in tidal volume, minute ventilation, peak inspiratory and expiratory flows, and inspiratory and expiratory drives. eNOS-/- male mice had smaller increases in minute ventilation, peak inspiratory flow and inspiratory drive, and smaller decreases in inspiratory time than WT males. Ventilatory responses in female eNOS-/- mice were similar to those in female WT mice. The ventilatory excitatory phase upon return to room-air was similar in both male and female WT mice. However, the post-HCC increases in frequency of breathing (with decreases in inspiratory times), and increases in tidal volume, minute ventilation, inspiratory drive (i.e., tidal volume/inspiratory time) and expiratory drive (i.e., tidal volume/expiratory time), and peak inspiratory and expiratory flows in male eNOS-/- mice were smaller than in male WT mice. In contrast, the post-HCC responses in female eNOS-/- mice were equal to those of the female WT mice. These findings provide the first evidence that the loss of eNOS affects the ventilatory responses during and after HCC in male C57BL6 mice, whereas female C57BL6 mice can compensate for the loss of eNOS, at least in respect to triggering ventilatory responses to HCC.

Effect of Continuous Positive Airway Pressure on the Ventilatory Response to CO2 in Preterm Infants

PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 634-638
Author(s):  
Manuel Durand ◽  
Ellen McCann ◽  
June P. Brady
Keyword(s):  
Tidal Volume ◽  
Preterm Infants ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Co2 Response ◽  
Expiratory Time ◽  
Ventilatory Response To Co2

The effect of continuous positive airway pressure (CPAP) on the ventilatory response to CO2 in newborn infants is unknown. The CO2 response to 4% CO2 in air was studied in nine preterm infants without lung disease before and during administration of CPAP (4 to 5 cm H2O) delivered by face mask. Minute ventilation, tidal volume, respiratory frequency, and end-tidal Pco2 were measured, and the slope and intercept of the CO2 response were calculated. Respiratory pattern and changes in oxygenation were also analyzed by measuring inspiratory and expiratory time, mean inspiratory flow, mean expiratory flow, effective respiratory timing, endtidal Po2, and transcutaneous Po2. CPAP significantly decreased minute ventilation from 278.7 to 197.6 mL/mm/kg (P &lt; .001). Tidal volume and respiratory frequency were also significantly decreased. The slope of the CO2 response during CPAP was not significantly different from the slope before CPAP (36 v 33 mL/min/kg/mm Hg, P &gt; .1), but the intercept was shifted to the right (P &lt; .001). The decrease in respiratory frequency was primarily due to a prolongation of expiratory time (P &lt; .05). In addition, transcutaneous Po2 increased during administration of CPAP (P &lt; .001). These findings indicate that: (1) CPAP significantly decreases ventilation in preterm infants without lung disease, affecting both tidal volume and respiratory frequency; (2) CPAP does not appreciably alter the ventilatory response to CO2; (3) the changes in respiratory frequency are primarily accounted for by a prolongation of expiratory time; (4) CPAP improves oxygenation.

Separation of factors responsible for change in breathing pattern induced by instrumentation

1985 ◽  
Vol 59 (5) ◽  
pp. 1515-1520 ◽  
Author(s):  
W. Perez ◽  
M. J. Tobin
Keyword(s):  
Tidal Volume ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Sensory Receptors ◽  
Inspiratory Time ◽  
Expiratory Time ◽  
Oral Breathing ◽  
Oral Stimulation ◽  
Additional Stimulation ◽  
Stimulation Of

Employment of mouthpiece and noseclips (MP + NC) has repeatedly been shown to increase tidal volume (VT), but its effect on respiratory frequency (f) and its subsets is controversial. The mechanisms accounting for this alteration in breathing pattern are poorly understood and may include stimulation of oral or nasal sensory receptors or alteration in the route of breathing. In this study we demonstrated that use of a MP + NC, compared with nonobtrusive measurement with a calibrated respiratory inductive plethysmograph, alters the majority of the volume and time indexes of breathing pattern, with increases in minute ventilation (P less than 0.01), VT (P less than 0.001), inspiratory time (TI, P less than 0.05), expiratory time (TE, P less than 0.05), mean inspiratory flow (P less than 0.05), and mean expiratory flow (P less than 0.05) and a decrease in f(P less than 0.05). Separating the potential mechanisms we found that when the respiratory route was not altered, independent oral stimulation (using an occluded MP) or nasal stimulation (by applying paper clips to the alae nasi) did not change the breathing pattern. In contrast, obligatory oral breathing without additional stimulation of the oral or nasal sensory receptors caused increases in VT (P less than 0.05), TI (P less than 0.05), and TE (P less than 0.01) and a fall in f(P less than 0.05). Heating and humidifying the inspired air did not prevent the alteration in breathing pattern with a MP. Thus change in the respiratory route is the major determinant of the alteration in breathing pattern with a MP + NC.

Role of the carotid bodies in chemosensory ventilatory responses in the anesthetized mouse

2004 ◽  
Vol 97 (4) ◽  
pp. 1401-1407 ◽  
Author(s):  
Masahiko Izumizaki ◽  
Mieczyslaw Pokorski ◽  
Ikuo Homma
Keyword(s):  
Tidal Volume ◽  
Carotid Body ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Whole Body ◽  
Sudden Increase ◽  
Ventilatory Responses ◽  
Carotid Bodies ◽  
Before And After ◽  
Carotid Body Denervation

We examined the effects of carotid body denervation on ventilatory responses to normoxia (21% O2 in N2 for 240 s), hypoxic hypoxia (10 and 15% O2 in N2 for 90 and 120 s, respectively), and hyperoxic hypercapnia (5% CO2 in O2 for 240 s) in the spontaneously breathing urethane-anesthetized mouse. Respiratory measurements were made with a whole body, single-chamber plethysmograph before and after cutting both carotid sinus nerves. Baseline measurements in air showed that carotid body denervation was accompanied by lower minute ventilation with a reduction in respiratory frequency. On the basis of measurements with an open-circuit system, no significant differences in O2 consumption or CO2 production before and after chemodenervation were found. During both levels of hypoxia, animals with intact sinus nerves had increased respiratory frequency, tidal volume, and minute ventilation; however, after chemodenervation, animals experienced a drop in respiratory frequency and ventilatory depression. Tidal volume responses during 15% hypoxia were similar before and after carotid body denervation; during 10% hypoxia in chemodenervated animals, there was a sudden increase in tidal volume with an increase in the rate of inspiration, suggesting that gasping occurred. During hyperoxic hypercapnia, ventilatory responses were lower with a smaller tidal volume after chemodenervation than before. We conclude that the carotid bodies are essential for maintaining ventilation during eupnea, hypoxia, and hypercapnia in the anesthetized mouse.

scholarly journals Electromagnetic inductance plethysmography is well suited to measure tidal breathing in infants

2016 ◽  
Vol 2 (4) ◽  
pp. 00062-2016 ◽  
Author(s):  
Mariann H.L. Bentsen ◽  
Morten Eriksen ◽  
Merete S. Olsen ◽  
Trond Markestad ◽  
Thomas Halvorsen
Keyword(s):  
Lung Function ◽  
Tidal Volume ◽  
Minute Ventilation ◽  
Ultrasonic Flowmeter ◽  
Tidal Breathing ◽  
Limits Of Agreement ◽  
Noninvasive Methods ◽  
Expiratory Time ◽  
Expiratory Flow ◽  
Mean Differences

Reliable, accurate and noninvasive methods for measuring lung function in infants are desirable. Electromagnetic inductance plethysmography has been used to perform infant spirometry and VoluSense Pediatrics (VSP) (VoluSense, Bergen, Norway) represents an updated version of this technique. We aimed to examine its accuracy compared to a validated system measuring airflow via a facemask using an ultrasonic flowmeter.We tested 30 infants with postmenstrual ages between 36 to 43 weeks and weights from 2.3 to 4.8 kg, applying both methods simultaneously and applying VSP alone. Agreement between the methods was calculated using Bland–Altman analyses and we also estimated the effect of applying the mask.Mean differences for all breathing parameters were within ±5.5% and limits of agreement between the two methods were acceptable, except perhaps for peak tidal expiratory flow (PTEF). Application of the facemask significantly increased tidal volume, minute ventilation, PTEF, the ratio of inspiratory to expiratory time and the ratio of expiratory flow at 50% of expired volume to PTEF.VSP accurately measured tidal breathing parameters and seems well suited for tidal breathing measurements in infants under treatment with equipment that precludes the use of a facemask.

Diaphragm and lung afferents contribute to inspiratory load compensation in awake ponies

1994 ◽  
Vol 76 (3) ◽  
pp. 1330-1339 ◽  
Author(s):  
H. V. Forster ◽  
T. F. Lowry ◽  
L. G. Pan ◽  
B. K. Erickson ◽  
M. J. Korducki ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Treadmill Exercise ◽  
Minute Ventilation ◽  
Inspiratory Time ◽  
Arterial Pco2 ◽  
Load Compensation ◽  
Expiratory Time ◽  
Inspiratory Load

We determined the effect of pulmonary vagal (hilar nerve) denervation (HND) and diaphragm deafferentation (DD) on inspiratory load compensation. We studied awake intact (I; n = 10), DD (n = 5), HND (n = 4), and DD+HND (n = 7) ponies at rest and during mild (1.8 mph, 5% grade) and moderate (1.8 mph, 15% grade) treadmill exercise before, during, and after resistance of the inspiratory circuit was increased from approximately 1.5 to approximately 20 cmH2O.l–1.s. During the first loaded breath in I ponies at rest, inspiratory time (TI) increased, expiratory time decreased, and inspiratory drive increased. There were minimal changes after the first breath, and inspiratory minute ventilation (VI) and arterial PCO2 did not change (P > 0.10) from control values. On the first loaded breath during exercise, TI increased but inspiratory drive either did not change or decreased from control values. TI and drive increased after the first breath, but the increases were insufficient to maintain VI and arterial PCO2 at control levels. First-breath load compensation remained after DD, HND, and DD+HND, but after DD+HND tidal volume and VI were compensated 5–10% less (P < 0.05) than in I ponies. In all groups inspiratory drive, tidal volume, and VI were markedly augmented on the first breath after loading was terminated with a gradual return toward control. We conclude that diaphragm and pulmonary afferents contribute to but are not essential for inspiratory load compensation in awake ponies.

Development of the ventilatory response to hypoxia in Swiss CD-1 mice

2000 ◽  
Vol 88 (5) ◽  
pp. 1907-1914 ◽  
Author(s):  
Dean M. Robinson ◽  
Henry Kwok ◽  
Brandon M. Adams ◽  
Karen C. Peebles ◽  
Gregory D. Funk
Keyword(s):  
Tidal Volume ◽  
Body Mass ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Developmental Changes ◽  
Hypoxic Exposure ◽  
Hypoxic Ventilatory Response ◽  
Expiratory Time ◽  
Ventilatory Response To Hypoxia

We examined developmental changes in breathing pattern and the ventilatory response to hypoxia (7.4% O2) in unanesthetized Swiss CD-1 mice ranging in age from postnatal day 0 to 42(P0–P42) using head-out plethysmography. The breathing pattern of P0 mice was unstable. Apneas were frequent at P0 (occupying 29 ± 6% of total time) but rare by P3 (5 ± 2% of total time). Tidal volume increased in proportion to body mass (∼10–13 ml/kg), but increases in respiratory frequency (f) (55 ± 7, 130 ± 13, and 207 ± 20 cycles/min for P0, P3, and P42, respectively) were responsible for developmental increases in minute ventilation (690 ± 90, 1,530 ± 250, and 2,170 ± 430 ml ⋅ min− 1 ⋅ kg− 1for P0, P3, and P42, respectively). Between P0 and P3, increases in f were mediated by reductions in apnea and inspiratory and expiratory times; beyond P3, increases were due to reductions in expiratory time. Mice of all ages showed a biphasic hypoxic ventilatory response, which differed in two respects from the response typical of most mammals. First, the initial hyperpnea, which was greatest in mature animals, decreased developmentally from a maximum, relative to control, of 2.58 ± 0.29 in P0 mice to 1.32 ± 0.09 in P42mice. Second, whereas ventilation typically falls to or below control in most neonatal mammals, ventilation remained elevated relative to control throughout the hypoxic exposure in P0 (1.73 ± 0.31), P3 (1.64 ± 0.29), and P9 (1.34 ± 0.17) mice but not in P19 or P42 mice.

Hyperoxic exposure affects the ventilatory response to hypoxia in awake rats

1988 ◽  
Vol 64 (1) ◽  
pp. 181-186 ◽  
Author(s):  
R. Arieli ◽  
D. Kerem ◽  
Y. Melamed
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Whole Body ◽  
Hyperoxic Exposure ◽  
Ventilatory Parameters ◽  
Ventilatory Drive ◽  
Co2 Balance ◽  
Hyperbaric O2 ◽  
Hyperbaric Exposure ◽  
Ventilatory Response To Hypoxia

We tested whether hyperbaric O2 (HBO) has an adverse effect on the hypoxic ventilatory drive. Four groups of rats were exposed for 550 min to O2 at 1.67, 1.90, and 2.15 ATA and to air at 1.90 ATA, respectively. Ventilatory parameters (frequency, tidal volume, and minute ventilation) were measured using whole-body plethysmography, before the hyperbaric exposure, immediately after the exposure, and up to 20 days after the exposure. Resting ventilation was not affected after exposure at 1.90 ATA to air or at 1.67 ATA to O2. HBO at 1.90 and 2.15 ATA caused a reduction of frequency and an elevation of tidal volume at different inspired gases: air, 5% CO2 balance O2, 80% O2, and 4.5% O2. However, minute ventilation on the day after the hyperoxic exposure was not different from the control at either air, 5% CO2, or 80% O2 but was markedly attenuated on the first three breaths at 4.5% O2. The hypoxic ventilation decreased to 48 +/- 13 (SD) and 32 + 11% after 1.90 and 2.15 ATA, respectively. The ventilatory parameters recovered in the days after HBO. We conclude that HBO reversibly depresses the hypoxic ventilatory drive, most probably by a direct effect on the carotid O2 chemoreceptors.

Effects of respiratory apparatus on breathing pattern

1980 ◽  
Vol 48 (4) ◽  
pp. 577-580 ◽  
Author(s):  
J. Askanazi ◽  
P. A. Silverberg ◽  
R. J. Foster ◽  
A. I. Hyman ◽  
J. Milic-Emili ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Tidal Volume ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Inspiratory Flow ◽  
Co2 Production ◽  
O2 Consumption ◽  
Expiratory Time ◽  
Respiratory Apparatus

The effects of ventilatory apparatus on breathing pattern and gas exchange were studied in normal supine subjects. Using a canopy system, measurements of O2 consumption, CO2 production, tidal volume (VT), frequency (f), minute ventilation, mean inspiratory flow, and inspiratory, and expiratory time (TI and TE) were made and compared to data obtained with the use of a mask (m) and mouthpiece plus noseclip (mp + nc). Use of the m or mp + nc caused a 32.5 and 15.5% increase in VT, respectively, whereas f, TI, and TE remained unchanged. As TI did not change the increase in VT was caused entirely by increased inspiratory flow.

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