TY - JOUR
T1 - Threshold altitude for bubble decay and stabilization in rat adipose tissue at hypobaric exposures
AU - Randsoe, Thomas
AU - Larsen, Ole Hyldegaard
PY - 2013/7
Y1 - 2013/7
N2 - Introduction: Bubble formation during altitude exposures, causing altitude decompression sickness (aDCS), has been referred to in theoretical models as venous gas embolisms (VGE). This has also been demonstrated by intravascular gas formation. Previous reports indicate that the formation of VGE and aDCS incidence increase abruptly for exposures exceeding 40-44 kPa ambient pressures. Further, extravascular micro air bubbles injected into adipose tissue grow transiently, then shrink and disappear while breathing oxygen (FIO2 = 1.0) at 71 kPa. At 25 kPa similar air bubbles will grow and stabilize during oxygen breathing without disappearing. We hypothesize that an ambient pressure threshold for either extravascular bubble stabilization or disappearance may be identified between 71 and 25 kPa. Whether extravascular bubbles will stabilize above a certain threshold has not been demonstrated before. Methods: In anesthetized rats, micro air bubbles (containing 79% nitrogen) of 500 nl were injected into exposed abdominal adipose tissue. Rats were decompressed in 2-35 min to either 60, 47, or 36 kPa and bubbles studied for 215 min during continued oxygen breathing (FIO2 = 1). Results: Significantly more bubbles shrank and disappeared at 60 (14 of 17) and 47 kPa (14 of 15) as compared to bubbles exposed to 36 kPa (3 of 15) ambient pressure. Conclusion: The results indicate that a threshold causing extravascular bubble stabilization or decay is between 47 to 36 kPa. The results are in agreement with previous reports demonstrating an increase in the formation of VGE and symptoms of aDCS at altitudes higher than 44 kPa ambient pressure.
AB - Introduction: Bubble formation during altitude exposures, causing altitude decompression sickness (aDCS), has been referred to in theoretical models as venous gas embolisms (VGE). This has also been demonstrated by intravascular gas formation. Previous reports indicate that the formation of VGE and aDCS incidence increase abruptly for exposures exceeding 40-44 kPa ambient pressures. Further, extravascular micro air bubbles injected into adipose tissue grow transiently, then shrink and disappear while breathing oxygen (FIO2 = 1.0) at 71 kPa. At 25 kPa similar air bubbles will grow and stabilize during oxygen breathing without disappearing. We hypothesize that an ambient pressure threshold for either extravascular bubble stabilization or disappearance may be identified between 71 and 25 kPa. Whether extravascular bubbles will stabilize above a certain threshold has not been demonstrated before. Methods: In anesthetized rats, micro air bubbles (containing 79% nitrogen) of 500 nl were injected into exposed abdominal adipose tissue. Rats were decompressed in 2-35 min to either 60, 47, or 36 kPa and bubbles studied for 215 min during continued oxygen breathing (FIO2 = 1). Results: Significantly more bubbles shrank and disappeared at 60 (14 of 17) and 47 kPa (14 of 15) as compared to bubbles exposed to 36 kPa (3 of 15) ambient pressure. Conclusion: The results indicate that a threshold causing extravascular bubble stabilization or decay is between 47 to 36 kPa. The results are in agreement with previous reports demonstrating an increase in the formation of VGE and symptoms of aDCS at altitudes higher than 44 kPa ambient pressure.
U2 - 10.3357/asem.3489.2013
DO - 10.3357/asem.3489.2013
M3 - Journal article
SN - 2375-6314
VL - 84
SP - 675
EP - 683
JO - Aerospace medicine and human performance
JF - Aerospace medicine and human performance
IS - 7
ER -