TY - JOUR
T1 - Impedance measurements of ex vivo rat lung at different volumes of inflation
AU - Oelze, Michael L.
AU - Miller, Rita J.
AU - Blue, James P.
AU - Zachary, James F.
AU - O'Brien, William D.
PY - 2003/12
Y1 - 2003/12
N2 - A previous study [J. Acoust. Soc. Am. 111, 1102-1109 (2002)] showed that the occurrence of ultrasonically induced lung hemorrhage in rats was directly correlated to the level of lung inflation. In that study, it was hypothesized that the lung could be modeled as two components consisting of air and parenchyma (contiguous tissue [pleura and septa]). The speed of sound and lung impedance would then depend on the fractional volume of air in the lung. According to that model, an inflated lung should act like a pressure-release surface for sound incident from tissue onto a tissue-lung boundary. A deflated lung containing less air should allow more acoustic energy into the lung tissue because the impedance was more closely matched to the contiguous tissues. In the study reported herein, a measurement technique was devised to calculate the impedance of seven rat lungs, ex vivo, under deflation (atmospheric pressure) and three volumes of inflation pressure (7-cm H2O, 10-cm H 2O, and 15-cm H2O). Lungs were dissected from rats and immediately scanned in a tank of degassed 37 °C water. The frequency-dependent acoustic pressure reflection coefficient was measured over a frequency range of 3.5 to 10 MHz. From the reflection coefficient, the frequency-dependent lung impedance was calculated with values ranging from an average of 1 Mrayls in deflated lungs to 0.2 Mrayls for fully inflated lungs. Lung impedance calculations showed that deflated lungs had an impedance closer to water (1.52 Mrayls) than inflated lungs. At all volumes of inflation, the lungs acted as pressure-release surfaces relative to the water. The average of the four lung impedance values (deflated, 7-cm H2O, 10-cm H 2O, and 15-cm H2O) at each level of inflation was statistically different (p<0.0001).
AB - A previous study [J. Acoust. Soc. Am. 111, 1102-1109 (2002)] showed that the occurrence of ultrasonically induced lung hemorrhage in rats was directly correlated to the level of lung inflation. In that study, it was hypothesized that the lung could be modeled as two components consisting of air and parenchyma (contiguous tissue [pleura and septa]). The speed of sound and lung impedance would then depend on the fractional volume of air in the lung. According to that model, an inflated lung should act like a pressure-release surface for sound incident from tissue onto a tissue-lung boundary. A deflated lung containing less air should allow more acoustic energy into the lung tissue because the impedance was more closely matched to the contiguous tissues. In the study reported herein, a measurement technique was devised to calculate the impedance of seven rat lungs, ex vivo, under deflation (atmospheric pressure) and three volumes of inflation pressure (7-cm H2O, 10-cm H 2O, and 15-cm H2O). Lungs were dissected from rats and immediately scanned in a tank of degassed 37 °C water. The frequency-dependent acoustic pressure reflection coefficient was measured over a frequency range of 3.5 to 10 MHz. From the reflection coefficient, the frequency-dependent lung impedance was calculated with values ranging from an average of 1 Mrayls in deflated lungs to 0.2 Mrayls for fully inflated lungs. Lung impedance calculations showed that deflated lungs had an impedance closer to water (1.52 Mrayls) than inflated lungs. At all volumes of inflation, the lungs acted as pressure-release surfaces relative to the water. The average of the four lung impedance values (deflated, 7-cm H2O, 10-cm H 2O, and 15-cm H2O) at each level of inflation was statistically different (p<0.0001).
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U2 - 10.1121/1.1624069
DO - 10.1121/1.1624069
M3 - Article
C2 - 14714818
AN - SCOPUS:0346847698
SN - 0001-4966
VL - 114
SP - 3384
EP - 3393
JO - Journal of the Acoustical Society of America
JF - Journal of the Acoustical Society of America
IS - 6 I
ER -