Journal of Ultrasound in Medicine, Vol 20, Issue 11 1197-1206, Copyright © 2001 by American Institute of Ultrasound in Medicine
Cardiopulmonary function in rats with lung hemorrhage induced by pulsed ultrasound exposure
J. M. Kramer, T. G. Waldrop, L. A. Frizzell, J. F. Zachary and W. D. O'Brien Jr
Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, 61801, USA.
OBJECTIVE: To assess cardiopulmonary function in rats exposed to pulsed
ultrasound using superthreshold exposure conditions known to produce
significant lung hemorrhage. METHODS: In 1 group of 9 anesthetized
Sprague-Dawley rats, 5 foci of ultrasound-induced hemorrhage were produced
in the left lung of each rat. In a second group of 6 rats, 5 foci of
ultrasound-induced hemorrhage were produced in the left and right lungs of
each rat. Each lesion was induced using superthreshold pulsed ultrasound
exposure conditions (3.1-MHz center frequency, 1.7-kHz pulse repetition
frequency, 1.3-micro-second pulse duration, 60-second exposure duration,
39-MPa in situ peak compressional pressure, and 17-MPa in situ peak
rarefactional pressure). After exposure, the lungs were fixed in formalin
and assessed histologically. The total lesion volume was calculated for
each lesion in each lung lobe. Measurements of cardiopulmonary function
included assessment of pulsatile arterial pressure, heart rate, end-tidal
carbon dioxide, respiratory rate, and arterial blood gases (PCO2 and PO2).
Functional data were quantified before (baseline) and 30 minutes after
exposure to ultrasound. RESULTS: In the 9 rats that had lesions in only the
left lung, the mean (SEM) lesion volume was 97 (13) mm3 and represented
about 3.4% of the total lung volume. In the 6 rats that had lesions in both
the left and right lungs, the left, right, and total mean lesion volumes,
respectively, were 102 (16), 114 (11), and 216 (18) mm3 and represented
about 3.7%, 4.2%, and 7.9% of the total lung volume. There were no
statistically significant differences in cardiopulmonary measurements
between baseline values and values obtained after exposure to ultrasound in
the 9 rats exposed on the left lung only. The 6 rats exposed bilaterally
had statistically significant differences in arterial pressure (134 +/- 4
versus 113 +/- 9 mm Hg; P= .047) and arterial PO2 (70 +/- 5 versus 58 +/- 4
mm Hg; P = .024) between baseline values and values obtained after exposure
to ultrasound. CONCLUSIONS: The severity of ultrasound-induced lesions
produced in 1 lung did not affect measurements of cardiopulmonary function
because of the functional respiratory reserve in the unexposed lung.
However, when both the left and right lungs had ultrasound-induced lesions,
the functional respiratory reserve was decreased to a point at which rats
were unable to maintain systemic arterial pressure or resting levels of
arterial PO2.
