Lesions of ultrasound-induced lung hemorrhage are not consistent with thermal injury - PubMed (original) (raw)

Comparative Study

Lesions of ultrasound-induced lung hemorrhage are not consistent with thermal injury

James F Zachary et al. Ultrasound Med Biol. 2006 Nov.

Abstract

Thermal injury, a potential mechanism of ultrasound-induced lung hemorrhage, was studied by comparing lesions induced by an infrared laser (a tissue-heating source) with those induced by pulsed ultrasound. A 600-mW continuous-wave CO2 laser (wavelength approximately 10.6 microm) was focused (680-microm beamwidth) on the surface of the lungs of rats for a duration between 10 to 40 s; ultrasound beamwidths were between 310 and 930 microm. After exposure, lungs were examined grossly and then processed for microscopic evaluation. Grossly, lesions induced by laser were somewhat similar to those induced by ultrasound; however, microscopically, they were dissimilar. Grossly, lesions were oval, red to dark red and extended into subjacent tissue to form a cone. The surface was elevated, but the center of the laser-induced lesions was often depressed. Microscopically, the laser-induced injury consisted of coagulation of tissue, cells and fluids, whereas injury induced by ultrasound consisted solely of alveolar hemorrhage. These results suggest that ultrasound-induced lung injury is most likely not caused by a thermal mechanism.

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Figures

Fig. 1

Fig. 1

Rat visceral pleura and the air–blood barrier. (a) The visceral pleural surface (P) of the rat lung is approximately 5 to 10 μm in thickness. It contains numerous capillaries (arrow), which separate it from the underlying air-filled alveolus (A). The box outlines the area of tissue demonstrated in Fig. 1b. Hematoxylin and eosin stain. Scale bar = 25 μm. (b) The illustration shows the area outlined by the box in Fig. 1a. The visceral pleural surface (P) of the rat lung is covered by a thin flat layer of mesothelial cells, is supported by fibrocytes and connective tissue and contains abundant capillaries (C). The air–blood barrier, formed by the endothelium of the capillary, basement membrane and type I pneumocytes (between the two arrows [this barrier varies in thickness, but has an arithmetic mean thickness of 1.25 μm, (Weibel and Knight (1964)]), is a point of impedance mismatch between the sound as it travels through tissue and fluids (blood) and abruptly hits the air in the alveolus (A). Inset: Higher magnification of the air–blood barrier (arrow head = endothelium). Transmission electron micrograph, lead citrate and uranyl acetate stain. Transmission electron micrograph courtesy of Dr. W. Haschek, Department of Pathobiology, University of Illinois.

Fig. 2

Fig. 2

Schematic diagram of the laser irradiation arrangement.

Fig. 3

Fig. 3

Constant temperature increase profiles of the laser irradiation of 65, 33 and 6.5° C, assuming that the temperature increase at the origin is 130° C. The laser beam's diameter(2wo) is 680 μm.

Fig. 4

Fig. 4

Ultrasound- and laser energy-induced lesions in rat lung. Gross lessons: (a) Ultrasound-induced lesions were consistent with hemorrhage, occurred under the visceral pleural and were oval and red to dark-red. (b) Laser energy-induced lesions were consistent with necrosis. Necrosis occurred through and under the visceral pleural, was oval and dark-red to brown. The pleural surface was injured as shown by the irregular depressed cavity in the center of the lesion. Microscopic (subgross) lesions: (c) With ultrasound, the lesion formed a “cone” of varied depths (see black lines), whose base was at the visceral pleural surface, the pleural surface was intact and elevated (hemorrhage) and the underlying alveoli were filled with hemorrhage (arrowhead = sample point for Fig. 4e). (d) With laser energy, the lesion also formed a “cone” of varied depths (see black lines) whose base was at the visceral pleural surface, the pleural surface was depressed and damaged (necrosis) and the underlying alveoli were coagulated (necrosis) (arrowhead = sample point for Fig. 4f). Microscopic lesions: (e) With ultrasound, lung had no visible lesions other than alveolar hemorrhage; (f) With laser energy, the pleura and septa were necrotic with coagulation of proteins (acute coagulative necrosis) and nucleic acid (nuclear pyknosis); and (g) Normal rat pleura and subjacent alveoli. Hematoxylin and eosin stain. Scale bar = 200 μm for Fig. 2c, d. Scale bar = 50 μm for Fig. 2e-g.

Fig. 5

Fig. 5

Laser energy-induced lesions in rat lung. (a) The pleura is homogeneous and light pink (tissue stains poorly with hematoxylin and eosin [H&E] stain) with retention of tissue architecture (necrosis). It also contains dead cells with clumped chromatin (nuclear pyknosis). This histopathologic appearance is also present in alveolar septa and there is some cellular debris in alveoli. Red blood cells in capillaries under the pleura and in alveolar septa are necrotic and their remnants form clear oval spaces (arrow). (b) At the margins of the necrotic tissue (conical shape) deep within the lung are intact (living) alveolar septa (tissue to the right of the line formed by the arrowheads) that contain abundant erythrocytes (active hyperemia). Alveolar septa with their red blood cells (arrows) are necrotic (tissue to the left of the line formed by the arrow-heads). H&E stain. Scale bar = 50 μm.

Fig. 6

Fig. 6

A simplified in vitro model for the region near the lung pleural surface is a water–air interface. The 6-cm diameter 3.32-MHz f/2.25 focused ultrasound source has a free-field pulse-echo −6-dB beam width at the focus of 6.7 mm. The focus is at the water–air interface. The free-field in vitro peak rarefactional pressures at the focus are 1.4 (top) and 1.8 (bottom) MPa. Their respective temporal-average intensities at the focus are 1.1 and 1.8 W/cm2. The pulse duration is 12.4 μs and the pulse repetition frequency is 1 kHz.

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