Ultrasonic Detection of Venous Gas Emboli and Tissue Gas in Rodents: Toward Imaging Biomarkers for Decompression Stress
Joshua B. CurrensiD, Katherine M. Eltz, Rani S. SellersiD, Emmanuel DugrenotiD, Virginie PapadopoulouiD
Abstract
Introduction In humans, decompression sickness (DCS) risk assessment often relies on surrogate ultrasound detection of venous gas emboli (VGE). Rodents are widely used to study DCS and mortality, yet no established relationship exists between imaging and decompression outcomes. We exposed rats to dives with differing DCS risk and investigated whether ultrasound measurements reflected modeled DCS risk and revealed tissue-level manifestations of decompression stress. Methods Rats underwent dry saturation exposures to 700 KPA in a hyperbaric chamber while breathing either heliox (low-risk; pDCS = 0.1%) or air (high-risk; pDCS = 13%), where pDCS was estimated using an existing rodent DCS risk model. Following decompression, animals were anesthetized for serial cardiac and renal ultrasound imaging. Echocardiograms were evaluated for VGE using an ordinal scale. The mean grayscale intensity (arbitrary units, a.u.) was also quantified in renal region of interest (ROI). In a separate set of animals, histopathology was conducted to evaluate renal manifestations. Results Observed peak VGE grades increased with estimated DCS risk, from grade 1 at pDCS 0.1% to grade 2 at pDCS 13%. Multi-organ analysis found lower renal ROI echogenicity during periods of high VGE, with mean grayscale intensities of 67.0 a.u. and 60.7 a.u. for VGE grades 0-1 and 2-4, respectively. Renal histopathology identified round voids consistent with pre-mortem gas emboli. Conclusions VGE burden tracked with pDCS risk. The decrease in renal image intensity during high VGE may indicate ultrasound attenuation from acoustic shadowing caused by excess tissue gas bubbles. These findings advance the development of physiologically relevant imaging biomarkers of decompression stress.
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