Modeling lung stretch in 3D could help reduce injuries for lungs on ventilators

Scilight ◽  
2021 ◽  
Vol 2021 (14) ◽  
pp. 141108
Author(s):  
Mara Johnson-Groh
Keyword(s):  
Lung Stretch

High oxygen concentrations predispose mouse lungsto the deleterious effects of high stretch ventilation

2003 ◽  
Vol 94 (3) ◽  
pp. 975-982 ◽  
Author(s):  
Timothy C. Bailey ◽  
Erica L. Martin ◽  
Lin Zhao ◽  
Ruud A. W. Veldhuizen
Keyword(s):  
Mechanical Ventilation ◽  
Acute Lung Injury ◽  
Lung Function ◽  
Lung Injury ◽  
Inflammatory Cytokines ◽  
Pulmonary Surfactant ◽  
Ex Vivo ◽  
Lung Stretch ◽  
Isolated Lungs ◽  
Mechanical Ventilation Group

Mechanical ventilation is a necessary intervention for patients with acute lung injury. However, mechanical ventilation can propagate acute lung injury and increase systemic inflammation. The exposure to >21% oxygen is often associated with mechanical ventilation yet has not been examined within the context of lung stretch. We hypothesized that mice exposed to >90% oxygen will be more susceptible to the deleterious effects of high stretch mechanical ventilation. C57B1/6 mice were randomized into 48-h exposure of 21 or >90% oxygen; mice were then killed, and isolated lungs were randomized into a nonstretch or an ex vivo, high-stretch mechanical ventilation group. Lungs were assessed for compliance and lavaged for surfactant analysis, and cytokine measurements or lungs were homogenized for surfactant-associated protein analysis. Mice exposed to >90% oxygen + stretch had significantly lower compliance, altered pulmonary surfactant, and increased inflammatory cytokines compared with all other groups. Our conclusion is that 48 h of >90% oxygen and high-stretch mechanical ventilation deleteriously affect lung function to a greater degree than stretch alone.

Interactions between lung stretch and PaCO2 in modulating ventilatory activity in dogs

1982 ◽  
Vol 53 (1) ◽  
pp. 185-191 ◽  
Author(s):  
G. S. Mitchell ◽  
B. A. Cross ◽  
T. Hiramoto ◽  
P. Scheid
Keyword(s):  
Pulmonary Artery ◽  
Airway Pressure ◽  
Artery Occlusion ◽  
Burst Frequency ◽  
Arterial Pco2 ◽  
Simple Effect ◽  
Burst Amplitude ◽  
Lung Stretch

The effects of changes in airway pressure (Paw) and arterial PCO2 (PaCO2) on ventilatory activity were studied in anesthetized thoracotomized dogs in which both lungs were ventilated separately. Pulmonary artery occlusion on one side and contralateral vagotomy allowed the reflex effects on ventilation of changes in Paw and PaCO2 to be elicited independently of each other. Ventilatory activity was assessed from integrated efferent phrenic activity, analyzed with respect to burst amplitude (Phr), burst frequency (f), and inspiratory TI) and expiratory duration (TE). While Phr increased linearly with PaCO2, it was independent of Paw. Both PaCO2 and Paw affected f in a complex nonadditive way; this response was entirely mediated by effects on TE, TI being unaffected by either stimulus. The analog of ventilation, estimated as Phr x f, increased linearly with PaCO2 and decreased linearly with Paw, but the effects of both stimuli appeared to be additive. It is concluded that the apparently simple effect of Paw and PaCO2 on ventilation results from more complex effects these stimuli exert on its components.

Contribution of lung stretch depressor reflex to nonlinear fall in cardiac output during PEEP

1984 ◽  
Vol 56 (6) ◽  
pp. 1578-1582 ◽  
Author(s):  
J. J. Schreuder ◽  
J. R. Jansen ◽  
A. Versprille
Keyword(s):  
Cardiac Output ◽  
Central Venous Pressure ◽  
Tidal Volume ◽  
Phase Ii ◽  
Venous Pressure ◽  
Gradual Decrease ◽  
Central Venous ◽  
Stretch Reflexes ◽  
Volume Phase ◽  
Lung Stretch

The hypothesis that lung stretch reflexes elicit negative cardiovascular effects during positive end-expiratory pressure (PEEP) application in a ramp procedure up to 15 cmH2O was tested in piglets under steady-state anesthesia and muscle relaxation. The effects of lung stretch on hemodynamics were studied by comparing the differences in responses during PEEP application with two different tidal volumes. In both ventilatory conditions cardiac output and aortic pressure decreased nonlinearly in three phases with the rise of PEEP: a gradual decrease in phase I, a sharp decrease in phase II, and again a more gradual decrease in phase III. Heart rate decreased significantly in phase II. In the series with the larger tidal volume, implying more lung stretch during insufflation, phase II was between a PEEP of 2.6 and 9 cmH2O. In the series with the smaller tidal volume, phase II occurred between 5.7 and 10.5 cmH2O. To assess the contribution of lung stretch reflexes to the decrease in cardiac output we also related cardiac output to the changes in central venous pressure. Again a nonlinear response was observed, indicating that an additional effect besides the rise in mean central venous pressure was involved in the decrease in cardiac output. During ventilation with the smaller tidal volume, phase II of the decrease in cardiac output was also shifted to higher values of mean central venous pressure, which only could be ascribed to the differences in lung stretch at insufflation. It appeared that under circumstances of artificial ventilation the onset of the reflex is determined by a characteristic threshold of lung stretch.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of naloxone on the hering-breuer apnea in sleeping kittens

1984 ◽  
Vol 56 (5) ◽  
pp. 1278-1282 ◽  
Author(s):  
C. M. Chow ◽  
D. J. Read
Keyword(s):  
Carotid Body ◽  
Sleep State ◽  
Endogenous Opiates ◽  
Apnea Duration ◽  
Lung Stretch ◽  
Medullary Neurons

The modulatory role of endogenous opiates on the Hering -Breuer inflation reflex was examined in 11 newborn kittens, aged 10–31 days, during active and quite sleep. The Hering -Breuer apnea duration was significantly shortened by naloxone (1 mg/kg, intraperitoneally; P less than 0.05). This effect was abolished by 100% O2 breathing. The duration of apnea, and its shortening by naloxone, did not differ significantly in the two sleep states. Hering -Breuer apnea is a result of the inspiratory inhibition and expiratory excitation of medullary neurons in response to lung stretch; the apnea is terminated by the opposing influences of chemoreceptors, which respond to hypercapnia and hypoxia. The results suggest that opioid influences on the Hering -Breuer reflex are due to an opioid modulation of the carotid body discharge in hypoxia, or of its central integration, and that sleep state is not implicated in such modulation in kittens.

Increase in breathing frequency following the reflex deep breath in anesthetized cats

1965 ◽  
Vol 20 (3) ◽  
pp. 491-495 ◽  
Author(s):  
Leslie B. Reynolds ◽  
Mata D. Hilgeson
Keyword(s):  
Mechanical Properties ◽  
Lung Compliance ◽  
Control Of Respiration ◽  
Breathing Frequency ◽  
Frequency Increase ◽  
Frequency Effects ◽  
Deep Breath ◽  
Lung Stretch ◽  
Frequency Changes ◽  
Dynamic Lung Compliance

In anesthetized cats, the inspiration-augmenting reflex, manifested as a spontaneous deep breath, was followed by a transient increase in breathing frequency in 66.5% of 382 cases observed. To determine whether this frequency increase was a property of altered mechanical properties of the lungs or was a property of the reflex itself, intact animals had their lungs inflated under conditions which would elicit the reflex as well as under conditions in which the reflex was absent. In all cases, dynamic lung compliance increased when the lungs were stretched. When the augmenting reflex was absent, breathing frequency decreased with increasing stretch. However, when the reflex occurred, breathing frequency increased to a maximum at a lung stretch of two and one-half times tidal volume. Frequency effects observed could be attributed to a combination of slowing by lung stretch and reflex speeding effects. The inspiration-augmenting reflex is proposed as a possible contributing mechanism to the tachypnea associated with lung conditions in which compliance is low. lung compliance; inspiration-augmenting reflex; breathing frequency changes; pulmonary airflow resistance; control of respiration; reflex tachypnea Submitted on May 18, 1964

scholarly journals Hypercapnia and Acidosis in Sepsis

2010 ◽  
Vol 112 (2) ◽  
pp. 462-472 ◽  
Author(s):  
Gerard Curley ◽  
Maya Contreras ◽  
Alistair D. Nichol ◽  
Brendan D. Higgins ◽  
John G. Laffey ◽  
...  
Keyword(s):  
Immune Response ◽  
Lung Injury ◽  
Therapeutic Potential ◽  
Adaptive Immune Response ◽  
Cytokine Signaling ◽  
Microbial Infection ◽  
Preclinical Models ◽  
Beneficial Effects ◽  
Lung Stretch ◽  
Substantial Morbidity

Acute respiratory distress syndrome is a devastating disease that causes substantial morbidity and mortality. Mechanical ventilation can worsen lung injury, whereas ventilatory strategies that reduce lung stretch, resulting in a "permissive" hypercapnic acidosis (HCA), improve outcome. HCA directly reduces nonsepsis-induced lung injury in preclinical models and, therefore, has therapeutic potential in these patients. These beneficial effects are mediated via inhibition of the host immune response, particularly cytokine signaling, phagocyte function, and the adaptive immune response. Of concern, these immunosuppressive effects of HCA may hinder the host response to microbial infection. Recent studies suggest that HCA is protective in the earlier phases of bacterial pneumonia-induced sepsis but may worsen injury in the setting of prolonged lung sepsis. In contrast, HCA is protective in preclinical models of early and prolonged systemic sepsis. Buffering of the HCA is not beneficial and may worsen pneumonia-induced injury.

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