Respiratory effects of progressive asphyxia in rabbit pups and adult rabbits

1984 ◽  
Vol 56 (4) ◽  
pp. 940-947 ◽  
Author(s):  
T. Trippenbach ◽  
R. Affleck ◽  
G. Kelly
Keyword(s):  
Time Course ◽  
Age Groups ◽  
Esophageal Pressure ◽  
Muscle Dysfunction ◽  
Respiratory Drive ◽  
Similar Time ◽  
Airway Occlusion ◽  
Temporal Relationships ◽  
Central Inspiratory Activity ◽  
Inspiratory Activity

Effects of prolonged airway occlusion were investigated in anesthetized and vagotomized 9-to 15-day-old pups and adult rabbits. The changes and temporal relationships between “integrated” phrenic activity, external intercostal electromyogram (INT), and esophageal pressure (Pes) were examined. Each occlusion resulted in hyperpnea, apnea, and gasping. Blood pressure recorded during the occlusion showed a marked decrease. During hyperpnea, the rate of changes and maximal amplitudes in Pes and INT were similar in both age groups. The increase in integrated phrenic activity (PHR) was significantly greater in young rabbits. In both age groups, changes in INT during gasping followed a similar time course and exceeded those in PHR. Maximal values of the three parameters were concurrent in adults, whereas the increase in INT peaked later than PHR and Pes in rabbit pups. In adult rabbits, PHR, INT, and Pes, during the last gasp, decreased to the values of the first hyperpnea breath. In rabbit pups, Pes of the last gasp decreased significantly below this value while INT was still elevated. This Pes decrease could result from inspiratory muscle dysfunction in the pups. Thus in rabbit pups, 1) greater changes in PHR were necessary to produce a given change in Pes than in adult rabbits; 2) activity of the external intercostal muscles was not efficient in developing pressure under conditions of asphyxia; and 3) the independent activation of diaphragmatic and intercostal motoneurons is not of vagal origin. Additionally, the results led us to conclude that Pes can serve as a close approximation of respiratory drive in adult rabbits. This parameter, however, cannot be used as an index of central inspiratory activity during gasping in rabbit pups.

scholarly journals Patient–ventilator asynchrony in acute brain-injured patients: a prospective observational study

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Xu-Ying Luo ◽  
Xuan He ◽  
Yi-Min Zhou ◽  
Yu-Mei Wang ◽  
Jing-Ran Chen ◽  
...  
Keyword(s):  
Prospective Observational Study ◽  
Esophageal Pressure ◽  
Respiratory Drive ◽  
Asynchrony Index ◽  
Mechanically Ventilated ◽  
Airway Occlusion ◽  
Brain Injured ◽  
Injured Patients ◽  
Duration Of Ventilation ◽  
Ventilated Patients

Abstract Background Patient–ventilator asynchrony is common in mechanically ventilated patients and may be related to adverse outcomes. Few studies have reported the occurrence of asynchrony in brain-injured patients. We aimed to investigate the prevalence, type and severity of patient–ventilator asynchrony in mechanically ventilated patients with brain injury. Methods This prospective observational study enrolled acute brain-injured patients undergoing mechanical ventilation. Esophageal pressure monitoring was established after enrollment. Flow, airway pressure, and esophageal pressure–time waveforms were recorded for a 15-min interval, four times daily for 3 days, for visually detecting asynchrony by offline analysis. At the end of each dataset recording, the respiratory drive was determined by the airway occlusion maneuver. The asynchrony index was calculated to represent the severity. The relationship between the prevalence and the severity of asynchrony with ventilatory modes and settings, respiratory drive, and analgesia and sedation were determined. Association of severe patient–ventilator asynchrony, which was defined as an asynchrony index  ≥ 10%, with clinical outcomes was analyzed. Results In 100 enrolled patients, a total of 1076 15-min waveform datasets covering 330,292 breaths were collected, in which 70,156 (38%) asynchronous breaths were detected. Asynchrony occurred in 96% of patients with the median (interquartile range) asynchrony index of 12.4% (4.3%–26.4%). The most prevalent type was ineffective triggering. No significant difference was found in either prevalence or asynchrony index among different classifications of brain injury (p > 0.05). The prevalence of asynchrony was significantly lower during pressure control/assist ventilation than during other ventilatory modes (p < 0.05). Compared to the datasets without asynchrony, the airway occlusion pressure was significantly lower in datasets with ineffective triggering (p < 0.001). The asynchrony index was significantly higher during the combined use of opioids and sedatives (p < 0.001). Significantly longer duration of ventilation and hospital length of stay after the inclusion were found in patients with severe ineffective triggering (p < 0.05). Conclusions Patient–ventilator asynchrony is common in brain-injured patients. The most prevalent type is ineffective triggering and its severity is likely related to a long duration of ventilation and hospital stay. Prevalence and severity of asynchrony are associated with ventilatory modes, respiratory drive and analgesia/sedation strategy, suggesting treatment adjustment in this particular population. Trial registration The study has been registered on 4 July 2017 in ClinicalTrials.gov (NCT03212482) (https://clinicaltrials.gov/ct2/show/NCT03212482).

Do canine scalene and sternomastoid muscles play a role in breathing?

1994 ◽  
Vol 76 (1) ◽  
pp. 242-252 ◽  
Author(s):  
A. De Troyer ◽  
M. Cappello ◽  
J. F. Brichant
Keyword(s):  
Respiratory Function ◽  
Respiratory Drive ◽  
Airway Occlusion ◽  
Single Breath ◽  
Large Numbers ◽  
Inspiratory Resistance ◽  
Cervical Vagotomy ◽  
Inspiratory Activity ◽  
Unanesthetized Animals ◽  
Spontaneously Breathing

To assess the respiratory function of the scalene and sternomastoid muscles in the dog, we studied the effect of graded increases in inspiratory airflow resistance and single-breath airway occlusion on the electrical activity of these muscles in 18 supine anesthetized spontaneously breathing animals. The sternomastoids never showed any activity, and the scalenes showed some inspiratory activity during occlusion in only two animals. The adoption of the prone position and bilateral cervical vagotomy did not affect this pattern. Hypercapnia also did not elicit any sternomastoid activity and induced scalene inspiratory activity during occlusion in only four of nine animals. On microscopic examination, however, both muscles were found to contain large numbers of spindles, suggesting that they have the capacity to respond to stretch. In addition, with increases in inspiratory resistance, both the sternum and ribs were displaced in the caudal direction. As a result, the scalenes demonstrated a gradual inspiratory lengthening and the normal inspiratory lengthening of the sternomastoids was accentuated. Additional studies in three unanesthetized animals showed consistent activity in the scalene and sternomastoid muscles during movements of the trunk and neck but no activity during breathing, including occluded breathing. These observations thus indicate that the alpha-motoneurons of the scalene and sternomastoid muscles in the dog have very small central respiratory drive potentials with respect to their critical firing threshold. In this animal, these muscles do not have a significant respiratory function.

Antagonistic interaction of laryngeal and central chemoreceptor respiratory reflexes

1992 ◽  
Vol 72 (2) ◽  
pp. 643-649 ◽  
Author(s):  
B. N. Van Vliet ◽  
M. Uenishi
Keyword(s):  
Superior Laryngeal Nerve ◽  
Control Mechanisms ◽  
Respiratory Drive ◽  
Absolute Level ◽  
Afferent Stimulation ◽  
Airway Reflex ◽  
Central Inspiratory Activity ◽  
Inspiratory Activity ◽  
The Right ◽  
Stimulation Of

Stimulation of laryngeal afferent fibers evokes a profound reflex inhibition of central respiratory drive. The interaction of this airway reflex with chemoreceptive ventilatory control mechanisms is poorly understood. The present study was undertaken to determine whether there is significant interaction between the effects of central chemoreceptor and laryngeal afferent stimulation on central inspiratory activity and, if so, to also determine the nature of the interaction. The effect of electrical stimulation of the superior laryngeal nerve (SLN) on the timing and intensity of central inspiratory activity was determined from the rectified and filtered phrenic neurogram in 10 dogs. Each dogs was decerebrated, artificially ventilated, vagotomized, and had the carotid bodies denervated. In each case, stimulation of the right SLN at 3 and 10 Hz caused a frequency-dependent slowing or arrest of central inspiratory activity. Increases in arterial PCO2 (PaCO2) attenuated the absolute level of inhibition of central inspiratory activity recorded during both SLN stimulation and control periods. Tp clarify the nature of the interaction between chemoreceptor and laryngeal afferent stimulation, the relationship between PaCO2 and central inspiratory activity was investigated during stimulation of the SLN at 0, 3, and 10 Hz. Control central inspiratory activity increased as a sigmoidal function of PaCO2. This sigmoidal relationship was greatly depressed during SLN stimulation but did not appear to be shifted along the PaCO2 axis. The results of this study therefore suggest that the interaction between central chemoreceptor and laryngeal afferent stimulation is multiplicative: the inhibition of the central inspiratory activity is mediated by an attenuation and not a resetting of central chemoreflexes.

Respiratory mechanics and timing during sleep in occlusive sleep apnea

1980 ◽  
Vol 48 (3) ◽  
pp. 432-437 ◽  
Author(s):  
R. J. Martin ◽  
B. E. Pennock ◽  
W. C. Orr ◽  
M. H. Sanders ◽  
R. M. Rogers
Keyword(s):  
Sleep Apnea ◽  
Cycle Time ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Respiratory Drive ◽  
Pulmonary Resistance ◽  
Airway Occlusion ◽  
Central Nervous System Activity ◽  
Gastric Pressure ◽  
Obese Subjects

Six human obese subjects with the sleep apnea hypersomnolence syndrome associated with upper airway occlusion (UAO) were studied during sleep to characterize respiration. Measurements included the timing components of ventilation, pulmonary resistance, flow, and esophageal and gastric pressures before and during UAOs. During the period between UAOs, the resistance progressively increased (9.4-18.1 cmH2O/l(-1) . s, P less than 0.05) as the ventilation decreased (1.82-0.77 l/s, P less than 0.05), but without changes in esophageal pressure swings. During this period, inspiratory time-to-total cycle time decreased (0.42-0.25 s, P less than 0.05) due to expiratory phase prolongation. The apnea began after expiration and terminated on inspiration with the maximal swings in esophageal and gastric pressure near the termination. During the UAO, the respiratory cycle time decreased slightly, but the expiratory pause time was significantly shortened immediately before ventilation. We suggest that the UAO is but one aspect of this syndrome and that a decrease in central nervous system activity diminishes the respiratory drive before the onset of the UAO.

Time course of phrenic activity and respiratory pressures during airway occlusion in cats

1981 ◽  
Vol 51 (1) ◽  
pp. 99-108 ◽  
Author(s):  
N. M. Siafakas ◽  
H. K. Chang ◽  
M. Bonora ◽  
H. Gautier ◽  
J. Milic-Emili ◽  
...  
Keyword(s):  
Time Course ◽  
Course Development ◽  
Airway Occlusion ◽  
Time Profiles ◽  
Inspiratory Muscles ◽  
Inspiratory Activity ◽  
Proportional Increase ◽  
Relationship Of ◽  
The Relationship ◽  
Hypoxic Mixtures

The morphology of integrated ("moving time average") phrenic electroneurograms (EPHR) and of tracheal (Ptr) and transdiaphragmatic (Pdi) pressure waves during occluded inspirations was studied in eight anesthetized cats breathing air and various hypercapnic and hypoxic mixtures. The shape of the rising part of EPR-, Ptr-, and Pdi-time profiles varied between animals (from convex to concave), but in each animal it remained virtually unchanged by hypoxia and hypercapnia. The shape of the Ptr and Pdi occlusion waves reflected the shape of EPHR. The relationship of EPHR to Pdi and Ptr did not change with chemical drive. It is concluded that central inspiratory activity (CIA) (as reflected by EPHR and its mechanical transforms Pdi and Ptr) increases in amplitude with stimulation of breathing but that the profile of CIA remains essentially unchanged. However, substantial differences in the time course development of phrenic activity, Pdi, and Ptr exist between cats. The fixed interrelationships among EPHR, Pdi, and Ptr indicate a proportional increase in activity among all inspiratory muscles with increased chemical drive.

Postnatal growth rate and gonadal development in circadian tau mutant hamsters reared in constant dim red light

Reproduction ◽  
2000 ◽  
pp. 327-330 ◽  
Author(s):  
RJ Lucas ◽  
JA Stirland ◽  
YN Mohammad ◽  
AS Loudon
Keyword(s):  
Time Course ◽  
Red Light ◽  
Somatic Growth ◽  
Postnatal Growth ◽  
Gonadal Development ◽  
Testicular Development ◽  
Wild Type ◽  
Similar Time ◽  
Syrian Hamsters ◽  
Body Weights

The role of the circadian clock in the reproductive development of Syrian hamsters (Mesocricetus auratus was examined in wild type and circadian tau mutant hamsters reared from birth to 26 weeks of age under constant dim red light. Testis diameter and body weights were determined at weekly intervals in male hamsters from 4 weeks of age. In both genotypes, testicular development, subsequent regression and recrudescence exhibited a similar time course. The age at which animals displayed reproductive photosensitivity, as exhibited by testicular regression, was unrelated to circadian genotype (mean +/- SEM: 54 +/- 3 days for wild type and 59 +/- 5 days for tau mutants). In contrast, our studies revealed a significant impact of the mutation on somatic growth, such that tau mutants weighed 18% less than wild types at the end of the experiment. Our study reveals that the juvenile onset of reproductive photoperiodism in Syrian hamsters is not timed by the circadian system.

scholarly journals Neurofilament Proteolysis after Focal Ischemia; When Do Cells Die after Experimental Stroke?

1999 ◽  
Vol 19 (6) ◽  
pp. 652-660 ◽  
Author(s):  
Jaroslaw Aronowski ◽  
Ki-Hyun Cho ◽  
Roger Strong ◽  
James C. Grotta
Keyword(s):  
Time Course ◽  
Infarct Volume ◽  
Focal Ischemia ◽  
Cellular Damage ◽  
Experimental Stroke ◽  
Infarct Core ◽  
Similar Time ◽  
The Core ◽  
Tetrazolium Staining ◽  
Previous Demonstration

To determine the occurrence and time-course of presumably irreversible subcellular damage after moderate focal ischemia, rats were subjected to 1, 3, 6, 9, or 24 hours of permanent unilateral middle cerebral and common carotid occlusion or 3 hours of reversible occlusion followed by 3, 6, or 21 hours of reperfusion. The topography and the extent of damage were analyzed with tetrazolium staining and immunoblot using an antibody capable of detecting breakdown of neurofilament. Neurofilament proteolysis began after 3 hours in the infarct core but was still incomplete in penumbral regions up to 9 hours. Similarly, tetrazolium-staining abnormalities were observed in the core of 50% of animals after 3 hours of ischemia. At 6 hours of permanent ischemia, infarct volume was maximal, and further prolongation of occlusion to 9 or 24 hours did not increase abnormal tetrazolium staining. In contrast to permanent ischemia and in agreement with the authors' previous demonstration of “reperfusion injury” in this model, prolongation of reperfusion from 3 hours to 6 and 21 hours after 3 hours of reversible occlusion gradually augmented infarct volume by 203% and 324%, respectively. Neurofilament proteolysis initiated approximately 3 hours after ischemia was quantitatively greatest in the core and extended during reperfusion to incorporate penumbra with a similar time course to that of tetrazolium abnormalities. These data demonstrate that, at least as measured by neurofilament breakdown and mitochondrial failure, extensive cellular damage is not present in penumbral regions for up to 9 hours, suggesting the potential for rescuing these regions by appropriate and timely neuroprotective strategies.

scholarly journals TGF-β1 increases permeability of ciliated airway epithelia via redistribution of claudin 3 from tight junction into cell nuclei

2021 ◽  
Author(s):  
Carolin Schilpp ◽  
Robin Lochbaum ◽  
Peter Braubach ◽  
Danny Jonigk ◽  
Manfred Frick ◽  
...  
Keyword(s):  
Time Course ◽  
Atopic Asthma ◽  
Ciliated Cells ◽  
Cell Nuclei ◽  
Tissue Remodelling ◽  
Similar Time ◽  
Airway Epithelia ◽  
Epithelial Integrity ◽  
Motile Cilia ◽  
Tgf Β1

AbstractTGF-β1 is a major mediator of airway tissue remodelling during atopic asthma and affects tight junctions (TJs) of airway epithelia. However, its impact on TJs of ciliated epithelia is sparsely investigated. Herein we elaborated effects of TGF-β1 on TJs of primary human bronchial epithelial cells. We demonstrate that TGF-β1 activates TGF-β1 receptors TGFBR1 and TGFBR2 resulting in ALK5-mediated phosphorylation of SMAD2. We observed that TGFBR1 and -R2 localize specifically on motile cilia. TGF-β1 activated accumulation of phosphorylated SMAD2 (pSMAD2-C) at centrioles of motile cilia and at cell nuclei. This triggered an increase in paracellular permeability via cellular redistribution of claudin 3 (CLDN3) from TJs into cell nuclei followed by disruption of epithelial integrity and formation of epithelial lesions. Only ciliated cells express TGF-β1 receptors; however, nuclear accumulations of pSMAD2-C and CLDN3 redistribution were observed with similar time course in ciliated and non-ciliated cells. In summary, we demonstrate a role of motile cilia in TGF-β1 sensing and showed that TGF-β1 disturbs TJ permeability of conductive airway epithelia by redistributing CLDN3 from TJs into cell nuclei. We conclude that the observed effects contribute to loss of epithelial integrity during atopic asthma.

scholarly journals Oxygen administration for patients with ARDS

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Shinichiro Ohshimo
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Positive Pressure ◽  
Respiratory Drive ◽  
Severe Hypoxemia ◽  
Airway Occlusion ◽  
Non Invasive ◽  
Oxygen Administration ◽  
Essential Interventions ◽  
Invasive Techniques

AbstractAcute respiratory distress syndrome (ARDS) is a fatal condition with insufficiently clarified etiology. Supportive care for severe hypoxemia remains the mainstay of essential interventions for ARDS. In recent years, adequate ventilation to prevent ventilator-induced lung injury (VILI) and patient self-inflicted lung injury (P-SILI) as well as lung-protective mechanical ventilation has an increasing attention in ARDS.Ventilation-perfusion mismatch may augment severe hypoxemia and inspiratory drive and consequently induce P-SILI. Respiratory drive and effort must also be carefully monitored to prevent P-SILI. Airway occlusion pressure (P0.1) and airway pressure deflection during an end-expiratory airway occlusion (Pocc) could be easy indicators to evaluate the respiratory drive and effort. Patient-ventilator dyssynchrony is a time mismatching between patient’s effort and ventilator drive. Although it is frequently unrecognized, dyssynchrony can be associated with poor clinical outcomes. Dyssynchrony includes trigger asynchrony, cycling asynchrony, and flow delivery mismatch. Ventilator-induced diaphragm dysfunction (VIDD) is a form of iatrogenic injury from inadequate use of mechanical ventilation. Excessive spontaneous breathing can lead to P-SILI, while excessive rest can lead to VIDD. Optimal balance between these two manifestations is probably associated with the etiology and severity of the underlying pulmonary disease.High-flow nasal cannula (HFNC) and non-invasive positive pressure ventilation (NPPV) are non-invasive techniques for supporting hypoxemia. While they are beneficial as respiratory supports in mild ARDS, there can be a risk of delaying needed intubation. Mechanical ventilation and ECMO are applied for more severe ARDS. However, as with HFNC/NPPV, inappropriate assessment of breathing workload potentially has a risk of delaying the timing of shifting from ventilator to ECMO. Various methods of oxygen administration in ARDS are important. However, it is also important to evaluate whether they adequately reduce the breathing workload and help to improve ARDS.

scholarly journals Pseudo-streaming potentials in Necturus gallbladder epithelium. II. The mechanism is a junctional diffusion potential.

1992 ◽  
Vol 99 (3) ◽  
pp. 317-338 ◽  
Author(s):  
L Reuss ◽  
B Simon ◽  
C U Cotton
Keyword(s):  
Time Course ◽  
Bathing Solution ◽  
Intercellular Spaces ◽  
Similar Time ◽  
Streaming Potentials ◽  
Osmotic Water ◽  
Lateral Intercellular Spaces ◽  
Transepithelial Voltage ◽  
Time Courses ◽  
Good Agreement

The mechanisms of apparent streaming potentials elicited across Necturus gallbladder epithelium by addition or removal of sucrose from the apical bathing solution were studied by assessing the time courses of: (a) the change in transepithelial voltage (Vms). (b) the change in osmolality at the cell surface (estimated with a tetrabutylammonium [TBA+]-selective microelectrode, using TBA+ as a tracer for sucrose), and (c) the change in cell impermeant solute concentration ([TMA+]i, measured with an intracellular double-barrel TMA(+)-selective microelectrode after loading the cells with TMA+ by transient permeabilization with nystatin). For both sucrose addition and removal, the time courses of Vms were the same as the time courses of the voltage signals produced by [TMA+]i, while the time courses of the voltage signals produced by [TBA+]o were much faster. These results suggest that the apparent streaming potentials are caused by changes of [NaCl] in the lateral intercellular spaces, whose time course reflects the changes in cell water volume (and osmolality) elicited by the alterations in apical solution osmolality. Changes in cell osmolality are slow relative to those of the apical solution osmolality, whereas lateral space osmolality follows cell osmolality rapidly, due to the large surface area of lateral membranes and the small volume of the spaces. Analysis of a simple mathematical model of the epithelium yields an apical membrane Lp in good agreement with previous measurements and suggests that elevations of the apical solution osmolality elicit rapid reductions in junctional ionic selectivity, also in good agreement with experimental determinations. Elevations in apical solution [NaCl] cause biphasic transepithelial voltage changes: a rapid negative Vms change of similar time course to that of a Na+/TBA+ bi-ionic potential and a slow positive Vms change of similar time course to that of the sucrose-induced apparent streaming potential. We conclude that the Vms changes elicited by addition of impermeant solute to the apical bathing solution are pseudo-streaming potentials, i.e., junctional diffusion potentials caused by salt concentration changes in the lateral intercellular spaces secondary to osmotic water flow from the cells to the apical bathing solution and from the lateral intercellular spaces to the cells. Our results do not support the notion of junctional solute-solvent coupling during transepithelial osmotic water flow.

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