Cardiopulmonary function in rats with lung hemorrhage induced by pulsed ultrasound exposure

Objective. To assess cardiopulmonary function in rats exposed to pulsed ult rasound using superthreshold exposure conditions known to produce significa nt lung hemorrhage. Methods. in 1 group of 9 anesthetized Sprague-Dawley ra ts, 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 hemo rrhage were produced in the left and right lungs of each rat. Each lesion w as 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 compressio nal pressure, and 17-MPa in situ peak rarefactional pressure). After exposu re, the lungs were fixed in formalin and assessed histologically. The total lesion volume was calculated for each lesion in each lung lobe. Measuremen ts of cardiopulmonary function included assessment of pulsatile arterial pr essure, heart rate, end-tidal carbon dioxide, respiratory rate, and arteria l blood gases (PCO2 and PO2). Functional data were quantified before (basel ine) and 30 minutes after exposure to ultrasound. Results. In the 9 rats th at had lesions in only the left lung, the mean (SEM) lesion volume was 97 ( 13) mm(3) and represented about 3.4% of the total lung volume. In the 6 rat s that had lesions in both the left and right lungs, the left, right, and t otal mean lesion volumes, respectively, were 102 (16), 114 (11), and 216 (1 8) mm(3) and represented about 3.7%, 4.2%, and 7.9% of the total lung volum e. There were no statistically significant differences in cardiopulmonary m easurements between baseline values and values obtained after exposure to u ltrasound in the 9 rats exposed on the left lung only. The 6 rats exposed b ilaterally had statistically significant differences in arterial pressure ( 134 +/- 4 versus 113 +/- 9 mm Hg; P = .047) and arrterial PO2 (70 +/- 5 ver sus 58 +/- 4 m m Hg; P = .024) between baseline values and values obtained after exposure to ultrasound. Conclusions. The severity of ultrasound-induc ed lesions produced in 1 lung did not affect measurements of cardiopulmonar y function because of the functional respiratory reserve-in the unexposed l ung. However, when both the left and right lungs had ultrasound-induced les ions, the functional respiratory reserve was decreased to a point at which rats were unable to maintain systemic arterial pressure or resting levels o f arterial PO2.