Gas embolization of the liver in a rat model of rapid decompression

Abstract

Occurrence of liver gas embolism after rapid decompression was assessed in 31 female rats that were decompressed in 12 min after 42 min of compression at 7 ATA ( protocol A). Sixteen rats died after decompression ( group I). Of the surviving rats, seven were killed at 3 h ( group II), and eight at 24 h ( group III). In group I, bubbles were visible in the right heart, aortic arch, liver, and mesenteric veins and on the intestinal surface. Histology showed perilobular microcavities in sinusoids, interstitial spaces, and hepatocytes. In g roup II, liver gas was visible in two rats. Perilobular vacuolization and significant plasma aminotransferase increase were present. In g roup III, liver edema was evident at gross examination in all cases. Histology showed perilobular cell swelling, vacuolization, or hydropic degeneration. Compared with basal, enzymatic markers of liver damage increased significantly. An additional 14 rats were decompressed twice ( protocol B). Overall mortality was 93%. In addition to diffuse hydropic degeneration, centrilobular necrosis was frequently observed after the second decompression. Additionally, 10 rats were exposed to three decompression sessions ( protocol C) with doubled decompression time. Their mortality rate decreased to 20%, but enzymatic markers still increased in surviving rats compared with predecompression, and perilobular cell swelling and vacuolization were present in five rats. Study challenges were 1) liver is not part of the pathophysiology of decompression in the existing paradigm, and 2) although significant cellular necrosis was observed in few animals, zonal or diffuse hepatocellular damage associated with liver dysfunction was frequently demonstrated. Liver participation in human decompression sickness should be looked for and clinically evaluated.

Post-dive ultrasound detection of gas in the liver of rats and scuba divers

“…The observed 53% mortality was in agreement with previous reports using the same dive proWle (L'Abbate et al 2010;WisloV and Brubakk 2001).…”

“…These Wndings challenged the existing paradigm that the liver is immune from gas embolism in DCS. In addition, our data showed evidence of zonal or diVuse hepatocellular damage from 3 to 24 h after decompression, associated with a signiWcant increase in enzymatic markers of liver damage (L'Abbate et al 2010).…”

“…At the end of the compression period, the rats were almost linearly decompressed to the 'surface' (100 kPa, 1 ATA) at a rate of 50 kPa min ¡1 (0.5 ATA). Using the above proWle of a simulated dive, we previously documented consistent gas bubble presence in the liver sinusoids by histologic examination, as well as increased biomarkers of liver dysfunction at 24 h upon decompression (L'Abbate et al 2010). The remaining four rats were not compressed in the hyperbaric chamber and represented the control group for echo imaging.…”

“…Chamber characteristics have previously been described (L'Abbate et al 2010). Animals were compressed at a rate of 200 kPa min ¡1 (2 ATA) to a Wnal pressure of 700 kPa (7 ATA), and maintained at that pressure for 42 min, breathing air.…”

A ternary model of decompression sickness in rats

“…Treatments and/or risk factors are then typically evaluated by the degree of difference in the proportion of animals that are diagnosed with DCS following decompression. 1 DCS in the rat has been variously defined and diagnostic criteria include survival time, [2][3][4] observable signs such as walking difficulties, 3,[5][6][7][8][9][10][11][12][13][14] paralysis, [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] rolling in a rotating cage, 5-9, 12, 13, 15, 16, 20 twitching/convulsions 5-9, 12, 13, 15, 16 and/or respiratory distress 5-7, 9-11, 13, 14, 17-19 .…”