Fibrinogenolysis in the absence of fibrin formation in severe hypobaric hypoxia.
Acute exposure to hypoxia causes acceleration of activated partial thromboplastin time (aPTT) and a rise in factor VIII precoagulant activity (F VIII:C). To determine whether this activation of coagulation leads to in vivo fibrin formation we investigated 15 army pilots before and at the end of 21 min (range 14-29) of hypobaric hypoxia. Mean final pressure in the decompression chamber was 283 (250-310) mm Hg causing a fall in oxygen saturation to 61.5% (53-69). Hypobaric hypoxia caused acceleration of thrombin time (p less than 0.05), aPTT (p less than 0.01), and euglobulin lysis time (p = 0.05), as well as a rise of F VIII:C (p less than 0.05), beta-thromboglobulin (p less than 0.005), fibrin(ogen) degradation products E (p less than 0.005) and B beta 15-42 (p less than 0.001), as well as lactate (p less than 0.001). Fibrinopeptide A, a marker of in vivo fibrin formation, did not change significantly. It is concluded that severe hypoxemia due to rapid decompression going to the limit of tolerance does not lead to fibrin formation, whereas the rise in fibrin(ogen) degradation products demonstrates activation of the fibrinolytic system.
Bärtsch
P
P
Department of Medicine, University of Bern, Switzerland.
Haeberli
A
A
Hauser
K
K
Gubser
A
A
Straub
P W
PW
D000328:Adult; D001273:Atmosphere Exposure Chambers; D001274:Atmospheric Pressure; D001777:Blood Coagulation; D002245:Carbon Dioxide / Q000378:metabolism; D005337:Fibrin / Q000378:metabolism*; D005340:Fibrinogen / Q000378:metabolism*; D005342:Fibrinolysis; D005344:Fibrinopeptide A / Q000032:analysis; D006400:Hematocrit; D006801:Humans; D008297:Male; D008889:Military Personnel; D010100:Oxygen / Q000502:physiology*; D010313:Partial Pressure; D001620:beta-Thromboglobulin / Q000032:analysis
D001620:beta-Thromboglobulin; D002245:Carbon Dioxide; D005344:Fibrinopeptide A; D005337:Fibrin; D005340:Fibrinogen; D010100:Oxygen