Das D K, Steinberg H, Bandyopadhyay D, Hoory S
Cardiovascular Laboratories, University of Connecticut School of Medicine, Farmington 06032.
J Nucl Med. 1988 May;29(5):657-62.
The early stages of microvascular injury are often difficult to detect due to the lack of a suitable marker to assess such an injury. We utilized the well known phenomenon of polymorphonuclear leukocyte (PMN) migration to the microvascular bed as a result of acute inflammatory reactions originating from the damaged cells. A radiotracer technique was developed, employing indium-111-labeled PMN for the detection of microvascular injury induced by hyperoxia. New Zealand white rabbits exposed to either 100% oxygen or air for various intervals of time were injected with indium-111-tropolone or oxine-labeled PMNs. Influx of radioactive PMN into the lung was detected in 72 hr/oxygen-exposed animals using gamma scintigraphic technique. Analysis of dry/wet ratios and histological examinations of the lung biopsies indicated noncardiogenic edema formation at this stage. Mortality was 50% beyond 96 hr/oxygen exposure. Our study thus provided a means to detect early microvascular injury during 72 hr/oxygen-exposure, which was not detectable by any other noninvasive techniques. The use of indium-111-labeled PMN thus appears to be a potentially important tool for the clinical assessment of lung microvascular injury.
由于缺乏合适的标志物来评估微血管损伤，其早期阶段往往难以检测。我们利用了众所周知的现象，即多形核白细胞（PMN）因受损细胞引发的急性炎症反应而迁移至微血管床。我们开发了一种放射性示踪技术，使用铟 - 111标记的PMN来检测高氧诱导的微血管损伤。将新西兰白兔暴露于100%氧气或空气中不同时间间隔，然后注射铟 - 111 - 托酚酮或肟标记的PMN。使用γ闪烁显像技术在暴露于氧气72小时的动物中检测到放射性PMN流入肺部。肺活检的干湿比分析和组织学检查表明在此阶段形成了非心源性水肿。暴露于氧气超过96小时的动物死亡率为50%。因此，我们的研究提供了一种在暴露于氧气72小时期间检测早期微血管损伤的方法，这是任何其他非侵入性技术无法检测到的。因此，使用铟 - 111标记的PMN似乎是临床评估肺微血管损伤的一种潜在重要工具。
