lung parenchymal strip
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2013 ◽  
Vol 186 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Michael J. Emery ◽  
Randy L. Eveland ◽  
Jin-Hye Min ◽  
Jacob Hildebrandt ◽  
Erik R. Swenson

1995 ◽  
Vol 78 (3) ◽  
pp. 1209-1209

Pages 2029–2035: M.S. Ludwig and M.J. Dallaire. “Structural composition of lung parenchymal strip and mechanical behavior during sinusoidal oscillation.” Page 2031, figure numbers were cited incorrectly: instead of Figs. 2–4, Figs. 2,4, and 5 should have been cited and instead of Figs. 5–7, Figs. 3,6, and 7 should have been cited. The text below contains the correct information.


1994 ◽  
Vol 77 (4) ◽  
pp. 2029-2035 ◽  
Author(s):  
M. S. Ludwig ◽  
M. J. Dallaire

The lung parenchymal strip is comprised of many different anatomic elements, including small vessels, small airways, and alveolar walls. We questioned whether the relative amounts of these different structures are important in determining the mechanical behavior of this preparation during dynamic oscillations. We studied 16 parenchymal strips (10 x 2 x 2 mm) from 12 Sprague-Dawley rats. The strips were suspended in an organ bath filled with Krebs solution, bubbled with 95% O2–5% CO2, and maintained at 37 degrees C. One end of the strip was attached to a force transducer, and the other end was attached to a lever system that effected length (L) changes. We oscillated the strips at various resting tensions (T) (0.9 and 1.5 g), frequencies (0.1, 0.3, 0.6, and 1.0 Hz), and amplitudes (1.1, 2.4, and 5.3% of optimal L). We obtained T vs. L curves and calculated the resistance, elastance, and hysteresivity (ratio of energy dissipated to energy stored) of the tissue. At the end of the experiment, the strips were fixed in Formalin at T = 1 g. Histological sections were examined, and the amounts of airway, blood vessel, and alveolar wall were quantified using point counting techniques. We found that whereas resistance varied significantly with frequency and T, elastance and hysteresivity varied with only T. The fractional areas of alveolar, blood vessel, and bronchial wall were 86.3 +/- 0.5 (SE), 8.4 +/- 0.3, and 5.3 +/- 0.4%. Only hysteresivity and the fractional area of alveolar wall were significantly correlated at the lower resting tension (r = -0.76, P = 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)


1994 ◽  
Vol 76 (2) ◽  
pp. 773-782 ◽  
Author(s):  
S. M. Mijailovich ◽  
D. Stamenovic ◽  
R. Brown ◽  
D. E. Leith ◽  
J. J. Fredberg

In fibrous connective tissue networks, mechanical loads may be transferred from one fiber to the next by friction between slipping fibers (J. Appl. Physiol. 74: 665–681, 1993). Here we tested that hypothesis; it predicts that elastance of fibrous networks increases with increasing frequency, decreases with increasing strain amplitude (delta epsilon), and decreases with tissue swelling by solvent. Similarly, it predicts that hysteresivity (eta) decreases with increasing frequency, increases with increasing delta epsilon, decreases with tissue swelling, and, importantly, exceeds that of isolated fibrous constituents of the matrix. Elastance and eta of two structurally dissimilar connective tissues were measured, the rabbit lung parenchymal strip (a loose collagenous tissue) and the pigeon ligamentum propatagiale (an elastin-rich tissue). Experiments covered the frequency range 0.03125-3.125 Hz. Elastance of lung parenchyma was substantially lower than that of propatagial ligament, increased linearly with the logarithm of frequency, and decreased with delta epsilon; that of ligamentum propatagiale was insensitive to both frequency and delta epsilon. eta of lung parenchyma decreased moderately with increasing frequency and assumed values of approximately 0.1, but eta of ligamentum propatagiale was frequency and delta epsilon invariant and assumed values an order of magnitude smaller. These tissues also showed disparate mechanical responses when exposed to hypertonic bath solutions. Although there were some quantitative differences between predictions and experimental observations, the dynamic behavior of lung parenchyma was generally consistent with that of a network in which load is transferred from one fiber to the next by the agency of friction acting at slipping interface surfaces.


1989 ◽  
Vol 41 (5) ◽  
pp. 357-359
Author(s):  
Maria L. Candenas ◽  
Elsa Anselmi

1989 ◽  
Vol 67 (5) ◽  
pp. 483-490 ◽  
Author(s):  
John F. Burka ◽  
Heather Briand ◽  
Peter Scott-Savage ◽  
Franco M. Pasutto

Arachidonic acid (AA) and ovalbumin (OA) were used to induce contractions of sensitized guinea pig tracheal spiral (indomethacin-pretreated) and lung parenchymal strip preparations. This model was used to examine the properties of three leukotriene (LT) D4 antagonists and a platelet-activating factor (PAF)–acether receptor antagonist. The three LTD4 antagonists, L-649,923, FPL 57231, and LY163443, inhibited AA-induced contractions of indomethacin-pretreated tracheal spirals selectively. The PAF–acether antagonist, L-652,731, did not inhibit AA-induced contractions of either trachea or parenchyma. This confirmed that AA-induced contractions of trachea involved release and activity of LTD4. The LTD4 antagonists and L-652,731 partially inhibited OA-induced contractions of both trachea and parenchyma. When L-649,923 and L-652,731 or FPL 57231 and L-652,731 were combined, an additive inhibitory effect on OA-induced contractions was observed. When LY163443 and L-652,731 were combined, the inhibitory effect was synergistic. This may be due to the additional effect of LY163443 to inhibit phosphodiesterase. Total inhibition of OA-induced contractions was obtainable with relatively low concentrations when a LTD4 and PAF–acether antagonist were combined. These results suggested that LTD4 and PAF–acether may be the two major mediators in our model of allergic bronchospasm. The LTD4 and PAF–acether antagonists had the capacity to decrease baseline tone, even on tissues that were already relaxed with indomethacin, suggesting that LTD4 and PAF–acether may contribute to intrinsic tone in airway smooth muscle.Key words: leukotriene D4, platelet-activating factor, airway smooth muscle, antagonists, allergic bronchospasm.


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