脉冲超声对大鼠肺损伤的影响

J. Zachary, L. Frizzell, W. O’Brien
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引用次数: 6

摘要

超声具有特殊的安全记录,但在小鼠、大鼠、兔子、猴子和猪的临床水平超声诱导肺出血的报道引起了人们的关注。本研究描述了脉冲超声(3.14 MHz, 1700 hz PRF, 1.4-/spl mu/s脉冲持续时间,60 s暴露时间,胸膜表面原位峰值分离压力为17 MPa,原位峰值压缩压力为39.7 MPa)诱导病变后肺的颞修复(愈合)反应。暴露后,于暴露后0、1、2、5、7、9、12、14和16天(dpe)评估肺部病变。对肺部的病变进行评分,数字化记录,并在10%福尔马林中固定。固定后,测量内脏胸膜表面各病变的尺寸。将病变切分并测量深度。时间变化表明红细胞通过加工和去除血红蛋白和铁色素而降解。显微病变与肉眼病变相似,修复反应导致肺结构的微小改变。肺的修复反应类似于与瘀伤相关的软组织的修复反应,但也有一个以梭形细胞局灶性增生为特征的增殖期,其表型有待确定。
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Lesion resolution following exposure of rat lung to pulsed ultrasound
Ultrasound has an exceptional safety record, but concerns have been raised by reports of clinical-level ultrasound-induced lung haemorrhage in mice, rats, rabbits, monkeys, and pigs. This study characterized the temporal reparative (healing) responses in lung following the induction of lesions by pulsed ultrasound (3.14 MHz, 1700-Hz PRF, 1.4-/spl mu/s pulse duration, 60-s exposure duration, in situ [at the pleural surface] peak rarefactional pressure of 17 MPa, and in situ peak compressional pressure of 39.7 MPa). Following exposure, lung lesions were evaluated at 0, 1, 2, 5, 7, 9, 12, 14, and 16 days post exposure (dpe). Lungs were scored for the presence of lesions, recorded digitally, and fixed in 10% formalin. After fixation, the dimensions of each lesion at the visceral pleural surface were measured. The lesions were bisected and the depth measured. The temporal changes were indicative of degradation of erythrocytes through processing and removal of hemoglobin and iron pigments. Microscopic lesions paralleled the gross lesions and reparative responses resulted in minimal alteration of lung structure. The reparative response in lung was analogous to reparative responses in soft tissues associated with bruising, but also had a proliferative phase characterized by focal hyperplasia of spindloid cells whose phenotypes need to be determined.
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