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Gilman B Allen

Publications and source records attributed to Gilman B Allen.

7 recordsLinked to original sources
PubMed2006

Choosing the frequency of deep inflation in mice: balancing recruitment against ventilator-induced lung injury.

Low tidal volume (Vt) ventilation is protective against ventilator-induced lung injury but can promote development of atelectasis. Periodic deep inflation (DI) can open the lung, but if delivered too frequently may cause damage via repeated overdistention. We therefore examined the effects of varying DI frequency on lung mechanics, gas exchange, and biomarkers of injury in mice. C57BL/6 males were mechanically ventilated with positive end-expiratory pressure (PEEP) of 2 cmH2O for 2 h. One high Vt group received a DI with each breath (HV). Low Vt groups received 2 DIs after each hour of ventilation (LV) or 2 DIs every minute (LVDI). Control groups included a nonventilated surgical sham and a group receiving high Vt with zero PEEP (HVZP). Respiratory impedance was measured every 4 min, from which tissue elastance (H) and damping (G) were derived. G and H rose progressively during LV and HVZP, but returned to baseline after hourly DI during LV. During LVDI and HV, G and H remained low and gas exchange was superior to that of LV. Bronchoalveolar lavage fluid protein was elevated in HV and HVZP but was not different between LV and LVDI. Lung tissue IL-6 and IL-1beta levels were elevated in HVZP and lower in LVDI compared with LV. We conclude that frequent DI can safely improve gas exchange and lung mechanics and may confer protection from biotrauma. Differences between LVDI and HV suggest that an optimal frequency range of DI exists, within which the benefits of maintaining an open lung outweigh injury incurred from overdistention.

Airway Resistance↗
PubMed2006

The estimation of lung mechanics parameters in the presence of pathology: a theoretical analysis.

Mechanical lung function is frequently assessed in terms of lung resistance (R (L)), lung elastance (E (L)), and airway resistance (R (aw)). These quantities are determined by measuring input impedance at various oscillation frequencies, and allow lung tissue resistance (R (t)) to be estimated as the difference between R (L) and R (aw). These various parameters change in characteristic ways in the presence of lung pathology. In particular, the ratio R (t)/E (L) (known as hysteresivity, (eta) has been shown both experimentally and in numerical simulations to increase when regional heterogeneities in mechanical function develop throughout the lung. In this study, we performed an analytical investigation of a two-compartment lung model and showed that while heterogeneity always leads to an increase in E (L), eta will increase only initially. When heterogeneity becomes extreme, eta stops increasing and starts to decrease. However, there are no experimental reports of eta decreasing under conditions in which heterogeneity would be expected to exist. We speculate that this is because liquid bridges invariably form across airway lumen that narrow to a certain point, thereby preventing them from achieving arbitrarily small non-zero radii. We also show that recruitment of closed lung units during lung inflation may lead to variables responses in both eta and E (L).

Airway Resistance↗
PubMed2006

A woman with cough, fever, and micronodular infiltrates on chest radiograph.

Hot tub lung is a form of hypersensitivity pneumonitis (HP) reported to be associated with exposure to large aerosolized inocula of Mycobacterium avium complex (MAC). Although the pathogenesis of the disease is still poorly understood, the pathology of MAC-related HP can be similar to that of sarcoidosis, with well-formed granulomas. We describe a patient with HP featuring well-formed granulomas on transbronchial biopsy specimens, a finding believed to be unique to MAC-related HP, also referred to as "hot tub lung".

Aged↗
PubMed2005

Pulmonary impedance and alveolar instability during injurious ventilation in rats.

The mechanical derangements in the acutely injured lung have long been ascribed, in large part, to altered mechanical function at the alveolar level. This has not been directly demonstrated, however, so we investigated the issue in a rat model of overinflation injury. After thoracotomy, rats were mechanically ventilated with either 1) high tidal volume (Vt) or 2) low Vt with periodic deep inflations (DIs). Forced oscillations were used to measure pulmonary impedance every minute, from which elastance (H) and hysteresivity (eta) were derived. Subpleural alveoli were imaged every 15 min using in vivo video microscopy. Cross-sectional areas of individual alveoli were measured at peak inspiration and end exhalation, and the percent change was used as an index of alveolar instability (%I-EDelta). Low Vt never led to an increase in %I-EDelta but did result in progressive atelectasis that coincided with an increase in H but not eta. DI reversed atelectasis due to low Vt, returning H to baseline. %I-EDelta, H, and eta all began to rise by 30 min of high Vt and were not reduced by DI. We conclude that simultaneous increases in both H and eta are reflective of lung injury in the form of alveolar instability, whereas an isolated and reversible increase in H during low Vt reflects merely derecruitment of alveoli.

Animals↗
PubMed2005

Acute lung injury: significance, treatment and outcome.

PURPOSE OF REVIEW: This paper aims to provide a condensed review of the most essential and current research findings in the field of acute lung injury over the past year. RECENT FINDINGS: We review the most recent important findings in both laboratory-based and clinical research in the field of acute lung injury. Significant advances have been made in the past year with respect to our understanding of the pathogenesis of acute lung injury, and how key pathological events relate to prognosis, outcomes, and the promise of new potential therapeutic interventions. In particular, significant advances have been made in our understanding of the prognostic roles of neutrophil recruitment and clearance, fibrinogenesis, inflammatory cytokines, alveolar fluid clearance, and endothelial injury and activation. Paramount studies have provided greater skepticism over the efficacy of prone positioning and the currently available surfactant replacement therapies. In addition, new research has fostered an improved appreciation of the long-term sequelae of acute lung injury. SUMMARY: Recent advances in our understanding of the pathogenesis of acute lung injury have provided the promise of exciting potential interventions to modify intravascular and extravascular fibrinogenesis, neutrophil activation and clearance, and alveolar fluid clearance. Our new understanding of prolonged disability and post-traumatic stress in acute lung injury survivors will ultimately change the standard for how these patients are managed in the intensive care unit and followed beyond their hospital stay.

Journal Article↗