High-frequency ventilation compared to conventional positive-pressure ventilation in the treatment of hyaline membrane disease in primates

Bell, Richard E.; Kuehl, Thomas J.; Coalson, Jacqueline J.; Ackerman, Neel B.; Null, Donald M.; Escobedo, Marilyn; Yoder, Bradley A.; Cornish, J. Devn; NALLE, LOUDEN; Skarin, Robert; Cipriani, Cheryl; Montes, Marisol; Robotham, James L.; deLemos, Robert A.

doi:10.1097/00003246-198409000-00017

Cited by 52 publications

(18 citation statements)

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“…This recovery presumably was associated with the appearance of functionally adequate levels of alveolar surfactant, was independent of ventilator mode, and occurred despite substantial differences in the magnitude and duration of oxygen exposure between the two ventilator groups. It is also consistent with our previous experience (17). From this we can conclude that the relative hyperoxia in the PPV/PEEP animals did not result in additive lung injury.…”

Section: Discussionsupporting

confidence: 93%

Ventilatory Management of Infant Baboons with Hyaline Membrane Disease: The Use of High Frequency Ventilation1

et al. 1987

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ABSTRAm. We tested the hypothesis that high frequency oscillatory ventilation (HFOV) would result in decreased pulmonary barotrauma in infants with hyaline membrane disease by comparing HFOV at 10 Hz to conventional positive pressure ventilation with continual distending airway pressure (PPV/PEEP) in premature baboons with hyaline membrane disease. Nineteen baboon fetuses were randomized to one of two treatment groups, delivered at 140 * 2 days, and, after stabilization and instrumentation of PPVIPEEP, placed in their respective ventilator group. Animals on conventional ventilation were managed by adjustment of tidal volume and frequency (to 1 Hz) to keep PaCOz below 55 and by adjustment of the mean airway pressure. One of the "HFOV" group died of cardiovascular complications before going on HFOV and was eliminated from data analysis. The remaining HFOV baboons survived the 11-day experimental period without evidence of airleak. Six of the 11 prematures treated with PPV/PEEP developed pulmonary interstitial emphysema and/or pneumothorax and five of the animals died within 48 h. The intergroup differences in airleak were significant (p < 0.05). Mean airway pressure (measured at the proximal airway) was higher initially with HFOV but then was lowered more rapidly than in the PPVIPEEP animals. The arterial to alveolar oxygen ratio rose and the FIOZ could be lowered more rapidly with HFOV than with conventional ventilation. These differences reached significance by 20 h. After 60 h there were no significant differences between HFOV and the PPVIPEEP survivors. HFOV resulted in more uniform saccular expansion, higher arterial to alveolar oxygen ratio, less oxygen exposure, and decreased acute barotrauma when compared to PPV/ PEEP. Although initially mean airway pressure was in the HFOV animals this was not associated with measurable baroinjury. These data support the efficacy of HFOV in the treatment of prematures with hyaline membrane disease. (Pediatr Res 21: 594-602, 1987) Abbreviations HFOV, high frequency oscillatory ventilation -Paw, mean airway pressure HMD, hyaline membrane disease Pa/A 02, arterial to alveolar oxygen ratio HFV, high frequency, low volume ventilation FawOz, FawC02, I:E, inspiratory:expiratory ratio ANOVA, analysis of variance PIE, pulmonary interstitial emphysema HFV has been proposed as an alternative to conventional PPV/PEEP in the management of infants with HMD (1-4). Interest in this technique has been generated by the observation that, with an appropriate strategy, HFV can accomplish gas exchange at lower intrapulmonary intraluminal distending pressures, thus potentially reducing the risk of baroinjury (5-8).The mechanisms of lung injury in infants with HMD are incompletely understood. Although most investigators believe that pulmonary immaturity, baroinjury, oxygen toxicity, and infection play a role in the pathogenesis of bronchopulmonary dysplasia, there is no general agreement about the relative importance of each factor (9-1 3). The premature baboon, delivered at 140 days gestatio...

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Section: Discussionsupporting

confidence: 93%

Ventilatory Management of Infant Baboons with Hyaline Membrane Disease: The Use of High Frequency Ventilation1

et al. 1987

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“…Details of routine nursery management are similar to those previously reported (3,13). In brief, a servo-controlled overhead radiant warmer was used to maintain core temperature, and i.v.…”

Section: Methodsmentioning

confidence: 99%

“…IMV animals (n = 8) were ventilated with a time-cycled, pressure-limited infant ventilator (Bear Cub, Bournes Inc., Riverside, CA) from the time of intubation. Pacoz was maintained within the target range by varying ventilatory frequency (initial 0.5 Hz, maximum 1 Hz) and tidal volume, with the inspiratory duration between 0.5 and 0.6 s. Based on previous experience, where higher ventilator pressures were associated with an extremely high incidence of airleak (13), PIP was initially set to maintain pa, at 1.2-1.3 kPa. To optimize lung volume and oxygenation, initial PEEP was set at 0.6-0.7 kPa and Fi02 was begun at 1 .O.…”

Section: Methodsmentioning

confidence: 99%

High-Frequency Oscillatory Ventilation Versus Intermittent Mandatory Ventilation: Early Hemodynamic Effects in the Premature Baboon with Hyaline Membrane Disease

Clark

et al. 1991

Pediatr Res

101

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ABSTRACT. We studied the hemodynamic consequences during the first 24 h of life in premature baboons (140 d) with hyaline membrane disease that were treated with high-frequency oscillatory ventilation (HFOV) or conventional intermittent mandatory ventilation (IMV). Cardiac output and organ blood flow were measured at three timepoints using the radiolabeled microsphere technique. Seven of seven HFOV and six of eight IMV animals survived_the 24-h period. By design, initial mean airway pressus (P,,) was higher in the HFOV group (p < 0.01). HFOV Pa, was progressively reduced during the study period because of improving oxygenation as measured by the arterial to alveolar oxygen ratio. In contrast, it was necessary to increase Paw in the IMV animals to maintain the arterial to alveolar oxygen ratio. By 23 h, the IMV group required higher Pa, than the HFOV group (p < 0.05) and had a lower arterial to alveolar oxygen ratio (p < 0.05). We found no significant differences in left ventricular output, effective systemic flow, organ blood flow, or central venous pressure between the two groups at 3, 8, or 23 h. The HFOV strategy used in our study resulted in significant improvement in oxygenation during the initial 24 h of treatment without adverse effect on left ventricular output, cerebral blood flow, or central venousjressure. We conclude that when appropriate changes in Pa, are made during HFOV in response to improvement in arterial oxgenation and changes in lung inflation as assessed by chest radiographs HFOV can be achieved without depressing cardiovascular dynamics more than during conventional therapy with IMV. (Pediatr Res 29: 160-166,1991) Abbreviations CVP, central venous pressure Fi02, fraction of inspired oxygen HFOV, high-frequency oscillatory ventilation HMD, hyaline membrane disease IMV, intermittent mandatory ventilation LVO, left ventricular output -Paw, mean airway pressure PEEP, positive end expiratory pressure PIP, peak inspiratory pressure

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“…Complete images of control and rCARDS toxin-treated lungs were obtained digitally using the Aperio Scanscope XT (Aperio, Vista, CA). Printed images of lungs from both study groups were graded for disease severity using a panel of standards (28,29).…”

Section: Histopathology and Immunohistochemistrymentioning

confidence: 99%

“…The mixed lymphocytic and eosinophilic mural infiltratrates persisted at the 14-day study period, but eosinophils were not evident in the perivascular lymphoid aggregates that dominated the 28-and 56-day lesions. The extent and severity of gross histological changes among the treatment groups were evaluated using the panel of standards method, with a grade 1 score being least severe and grade 5 score being most severe (28,29). Images of the graded standards used in this analysis are presented Figures E2A through E2E in the online supplement.…”

Section: Rcards Toxin Induces a Mixed Eosinophilic-lymphocytic Inflammentioning

confidence: 99%

Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation

Medina¹,

Coalson²,

Brooks

et al. 2012

Am J Respir Cell Mol Biol

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Mycoplasma pneumoniae causes acute and chronic lung infections in humans, leading to a variety of pulmonary and extrapulmonary sequelae. Of the airway complications of M. pneumoniae infection, M. pneumoniae-associated exacerbation of asthma and pediatric wheezing are emerging as significant sources of human morbidity. However, M. pneumoniae products capable of promoting allergic inflammation are unknown. Recently, we reported that M. pneumoniae produces an ADP-ribosylating and vacuolating toxin termed the community-acquired respiratory distress syndrome (CARDS) toxin. Here we report that naive mice exposed to a single dose of recombinant CARDS (rCARDS) toxin respond with a robust inflammatory response consistent with allergic disease. rCARDS toxin induced 30-fold increased expression of the Th-2 cytokines IL-4 and IL-13 and 70-to 80-fold increased expression of the Th-2 chemokines CCL17 and CCL22, corresponding to a mixed cellular inflammatory response comprised of a robust eosinophilia, accumulation of T cells and B cells, and mucus metaplasia. The inflammatory responses correlate temporally with toxin-dependent increases in airway hyperreactivity characterized by increases in airway restriction and decreases in lung compliance. Furthermore, CARDS toxin-mediated changes in lung function and histopathology are dependent on CD4 1 T cells. Altogether, the data suggest that rCARDS toxin is capable of inducing allergic-type inflammation in naive animals and may represent a causal factor in M. pneumoniae-associated asthma.Keywords: Mycoplasma pneumoniae; asthma; rCARDS toxin; eosinophilia; T cell Mycoplasma pneumoniae is a common human bacterial pathogen that causes acute and chronic infections of the respiratory tract and extrapulmonary pathology (1, 2). With the exception of mycoplasma adherence to the host epithelium, molecular mechanisms of virulence associated with the pathogenesis of M. pneumoniae infection are not well understood (1, 3). M. pneumoniae is predominantly an extracellular pathogen that binds to respiratory epithelial cells using a polarized tip organelle (1, 3-5). Interaction of M. pneumoniae with the respiratory epithelium results in significant cytopathology in cell culture and in vivo (4, 5). Previously, the cytopathology was attributed in part to the cytotoxic effects of hydrogen peroxides produced by M. pneumoniae (3). However, recently, we identified an ADP-ribosylating and vacuolating toxin produced by M. pneumoniae that is capable of inducing cytopathology in vitro and in vivo and that reproduces the infectious process (6-9).The community-acquired respiratory distress syndrome (CARDS) toxin encoded by the MPN372 gene was functionally identified as a human surfactant protein A binding protein (7). Upon further investigation, we discovered that CARDS toxin possesses structurally and functionally important regions of identity to the pertussis toxin S1 protein. Furthermore, highly purified rCARDS toxin causes extensive dose-dependent cytopathology in mammalian cell and organ culture, suggestin...

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High-frequency ventilation compared to conventional positive-pressure ventilation in the treatment of hyaline membrane disease in primates

Cited by 52 publications

References 0 publications

Ventilatory Management of Infant Baboons with Hyaline Membrane Disease: The Use of High Frequency Ventilation1

Ventilatory Management of Infant Baboons with Hyaline Membrane Disease: The Use of High Frequency Ventilation1

High-Frequency Oscillatory Ventilation Versus Intermittent Mandatory Ventilation: Early Hemodynamic Effects in the Premature Baboon with Hyaline Membrane Disease

Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation

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