Comparative Quantitative Morphology of the Mammalian Lung: Diffusing Area

Tenney, S.M.; Remmers, John E.

doi:10.1038/197054a0

Cited by 349 publications

(138 citation statements)

References 6 publications

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“…It is, however, worth noting that the use of V T /kg body weight as a surrogate for lung strain holds true only if FRC is linearly correlated with body mass among different mammals. Unfortunately, although preliminary studies have indicated such a correlation [18], FRC appears to be correlated rather with body weight to the power 1.13 [19]. This indicates that in smaller animals, lung resting volume is smaller than in larger animals, in proportion to their body mass, as also confirmed by our data (power 1.25 by allometric analysis, r 2 = 0.99, p = 0.0001, see Fig.…”

Section: Discussionsupporting

confidence: 85%

Time to generate ventilator-induced lung injury among mammals with healthy lungs: a unifying hypothesis

et al. 2011

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Purpose: To investigate ventilator-induced lung injury (VILI), several experimental models were designed including different mammalian species and ventilator settings, leading to a large variability in the observed time-course and injury severity. We hypothesized that the time-course of VILI may be fully explained from a single perspective when considering the insult actually applied, i.e. lung stress and strain. Methods: Studies in which healthy animals were aggressively ventilated until preterminal VILI were selected via a Medline search. Data on morphometry, ventilator settings, respiratory function and duration of ventilation were derived. For each animal group, lung stress (transpulmonary pressure) and strain (endinspiratory lung inflation/lung resting volume ratio) were estimated. Results: From the Medline search 20 studies including five mammalian species (sheep, pigs, rabbits, rats, mice) were selected. Time to achieve preterminal VILI varied widely (18-2,784 min), did not correlate with either tidal volume (expressed in relation to body weight) or airway pressure applied, but was weakly associated with lung stress (r 2 = 0.25, p = 0.008). In contrast, the duration of mechanical ventilation was closely correlated with both lung strain (r 2 = 0.85, p \ 0.0001) and lung strain weighted for the actual time of application during each breath (r 2 = 0.83, p \ 0.0001), according to exponential decay functions. When it was normalized for the lung strain applied, larger species showed a greater resistance to VILI than smaller species (medians, 25th-75th percentiles: 690, 460-2,001 min vs. 16, 4-59 min, respectively; p \ 0.001). Conclusion: Lung strain may play a critical role as a unifying rule describing the development of VILI among mammals with healthy lungs.

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Section: Discussionsupporting

confidence: 85%

Time to generate ventilator-induced lung injury among mammals with healthy lungs: a unifying hypothesis

et al. 2011

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“…Not only is there a lack of strain-specific alveolar diameters, but also strain-specific morphological shape data are not available. For example, Tenney and Reemers (1963) reported a 46.6-mm mouse alveolar diameter compared with the 58-mm mouse alveolar diameter reported by Mercer et al (1994) that was used in this study. Although the strain of mouse used was not specified by either author, we chose to use the Mercer et al (1994) data due to the rigorous morphological techniques used in this study.…”

Section: Discussionmentioning

confidence: 77%

Predicted Tracheobronchial and Pulmonary Deposition in a Murine Asthma Model

Oldham

Robinson

2007

The Anatomical Record

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Particulate matter dosimetry provides the critical link between exposures and initial doses reaching various sites in the respiratory tract. To extrapolate findings from animal models to humans, quantitative respiratory-tract anatomical data dosimetry in these animal models is required. The goal of this study was to provide anatomical information for the tracheobronchial and pulmonary region so predictions of particle deposition could be performed for a widely used model of asthma; the sensitized Balb/c mouse. Tracheobronchial airway morphometry of sensitized male Balb/c mice was generated from three in situ prepared lung casts. Distribution of the number of generations to terminal bronchiole for each lung lobe was determined by assigning a unique binary number to each airway. This strategy enabled the median path length to terminal bronchiole to be determined. A total of 25 median length paths to terminal bronchiole were measured (airway length, diameter, and branch angle) in each lung cast. These 25 paths were proportionately distributed among the six lobes based upon the number of median length pathways in each cast. Airway length, diameter, and branch angle were measured for each airway in the 25 median length pathways. Measurements of airway length, diameter, and branch angle for each generation were averaged to create a typical path tracheobronchial anatomy model. A pulmonary airway model was also developed so that particle deposition predictions could be performed for particle diameters of 0.2-10 micrometers. Particle deposition efficiency predictions were consistent with in vivo measured deposition.

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“…We can estimate the number of alveoli supplied by each vessel of this size by dividing the total number of alveoli in the lung by the total number of 30-m arterioles. Data for this calculation are available for dog lungs, for which we calculate a ratio of 750 alveoli per 30-m arteriole (13,14). We assume a similar ratio for rat lungs.…”

Section: Effect Of Parenchyma On Particle Distributionmentioning

confidence: 99%

“…Assuming that a rat alveolus has an average diameter of 75 m, the lowpower map dimensions (Fig. 1) measured ϳ90 ϫ 45 ϫ 1.3 alveoli (14). This is appropriate for evaluating interalveolar perfusion distribution.…”

Section: Effect Of Parenchyma On Particle Distributionmentioning

confidence: 99%

Perfusion heterogeneity in rat lungs assessed from the distribution of 4-μm-diameter latex particles

Conhaim

Watson

Heisey

et al. 2003

Journal of Applied Physiology

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sion heterogeneity in rat lungs assessed from the distribution of 4-m-diameter latex particles. J Appl Physiol 94: 420-428, 2003. First published October 11, 2002 10.1152/japplphysiol. 00700.2002.-Pulmonary vascular perfusion has been shown to follow a fractal distribution down to a resolution of 0.5 cm 3 (5E11 m 3 ). We wanted to know whether this distribution continued down to tissue volumes equivalent to that of an alveolus (2E5 m 3 ). To investigate this, we used confocal microscopy to analyze the spatial distribution of 4-m-diameter fluorescent latex particles trapped within rat lung microvessels. Particle distributions were analyzed in tissue volumes that ranged from 1.7E2 to 2.8E8 m 3 . The analysis resulted in fractal plots that consisted of two slopes. The left slope, encompassing tissue volumes less than 7E5 m 3 , had a fractal dimension of 1.50 Ϯ 0.03 (random distribution). The right slope, encompassing tissue volumes greater than 7E5 m 3 , had a fractal dimension of 1.29 Ϯ 0.04 (nonrandom distribution). The break point at 7E5 m 3 corresponds closely to a tissue volume equivalent to that of one alveolus. We conclude that perfusion distribution is random at tissue volumes less than that of an alveolus and nonrandom at tissue volumes greater than that of an alveolus. alveolar perfusion; fluorescent microspheres; fractal analysis; pulmonary blood flow FRACTAL ANALYSIS HAS BEEN used extensively to analyze the distribution of perfusion throughout the lung (3). The method is to infuse 15-m-diameter fluorescent latex particles into the pulmonary circulation and then count the number of trapped particles in blocks of frozen or air-dried lungs (15). The blocks, which range in size from 0.5 mm 3 to 2 cm 3 , are grouped mathematically to allow particle counts to be obtained in successive volumes of tissue that range from single tissue blocks up to groups of blocks on the scale of the whole lung (4). For groups of each volume, the mean and SD of the particle counts are calculated for the blocks that compose the group. A fractal plot is assembled by plotting the log of the coefficient of variation (CV; SD/mean) of the group count against the log of the group tissue volume. When this is done for groups of all volumes, it produces a linear plot that shows that the CV of the particle count increases as the group tissue volume decreases. The linearity of such plots is considered to be evidence of a fractal system, which means that perfusion distribution within the lung follows a fractal pattern. Fractals are complex geometric shapes that exhibit a scale-independent property of self-similarity such that the smallest part, no matter how highly magnified, resembles the whole (11). Using this approach, Glenny and colleagues (4) showed that pulmonary perfusion distribution remained fractal down to a tissue volume of 0.5 cm 3 (5E11 m 3 ).It is interesting to speculate whether or not this pattern continues down to the level of the alveolus. An alveolus with a diameter of 75 m has a volume of 2.2E5 m 3 , but present methods...

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Comparative Quantitative Morphology of the Mammalian Lung: Diffusing Area

Cited by 349 publications

References 6 publications

Time to generate ventilator-induced lung injury among mammals with healthy lungs: a unifying hypothesis

Time to generate ventilator-induced lung injury among mammals with healthy lungs: a unifying hypothesis

Predicted Tracheobronchial and Pulmonary Deposition in a Murine Asthma Model

Perfusion heterogeneity in rat lungs assessed from the distribution of 4-μm-diameter latex particles

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