title: Cardiopulmonary function in rats with lung hemorrhage induced by pulsed ultrasound exposure.
abstract: 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.
authors.affiliation: Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, 61801, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: Kramer
authors.forename: T G
authors.initials: TG
authors.lastname: Waldrop
authors.forename: L A
authors.initials: LA
authors.lastname: Frizzell
authors.forename: J F
authors.initials: JF
authors.lastname: Zachary
authors.forename: W D
authors.initials: WD
authors.lastname: O'Brien
mesh_terms: D000818:Animals; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D006470:Hemorrhage / Q000209:etiology* / Q000503:physiopathology*; D008171:Lung Diseases / Q000209:etiology* / Q000503:physiopathology*; D055370:Lung Injury; D051381:Rats; D017207:Rats, Sprague-Dawley; D012119:Respiration; D014465:Ultrasonics / Q000009:adverse effects*