fibrin and Altitude-Sickness

fibrin has been researched along with Altitude-Sickness* in 2 studies

Trials

1 trial(s) available for fibrin and Altitude-Sickness

Article	Year
Does altitude or exercise induce fibrin degradation in mountaineers? Journal of the Royal Society of Medicine, 1995, Volume: 88, Issue:4 Topics: Adult; Altitude; Altitude Sickness; Cross-Over Studies; Exercise; Fibrin; Humans; Male	1995

Other Studies

1 other study(ies) available for fibrin and Altitude-Sickness

Article	Year
Enhanced fibrin formation in high-altitude pulmonary edema. Journal of applied physiology (Bethesda, Md. : 1985), 1987, Volume: 63, Issue:2 Blood coagulation, fibrinolysis, and arterial blood gases were examined in 66 nonacclimatized mountaineers at 4,557 m. Subjects were classified according to a clinical score as healthy (n = 25), having mild acute mountain sickness (AMS) (n = 24), showing severe AMS (n = 13), and suffering from high-altitude pulmonary edema (HAPE) (n = 4). Coagulation times, euglobulin lysis time, and fibrin(ogen) fragment E were normal in all groups without significant changes. Fibrinopeptide A (FPA), a molecular marker of in vivo fibrin formation, was elevated in HAPE to 4.2 +/- 2.7 ng/ml (P less than 0.0001) compared with the other groups showing mean values between 1.6 +/- 0.4 and 1.8 +/- 0.7 ng/ml. FPA was normal in one patient with HAPE, however. Severe AMS was accompanied by a significant decrease in arterial PO2 due to an increase in alveolar-arterial O2 difference, whereas arterial PCO2 did not change significantly. We conclude that activation of blood coagulation is not involved in the pathogenesis of AMS and the impairment of gas exchange in this disease. Fibrin generation occurring in HAPE is probably an epiphenomenon of edema formation. Topics: Adult; Altitude Sickness; Arteries; Blood Coagulation; Blood Gas Analysis; Female; Fibrin; Humans; Hypoxia; Male; Pulmonary Edema	1987

Article

Year

Enhanced fibrin formation in high-altitude pulmonary edema.

Journal of applied physiology (Bethesda, Md. : 1985), 1987, Volume: 63, Issue:2

Blood coagulation, fibrinolysis, and arterial blood gases were examined in 66 nonacclimatized mountaineers at 4,557 m. Subjects were classified according to a clinical score as healthy (n = 25), having mild acute mountain sickness (AMS) (n = 24), showing severe AMS (n = 13), and suffering from high-altitude pulmonary edema (HAPE) (n = 4). Coagulation times, euglobulin lysis time, and fibrin(ogen) fragment E were normal in all groups without significant changes. Fibrinopeptide A (FPA), a molecular marker of in vivo fibrin formation, was elevated in HAPE to 4.2 +/- 2.7 ng/ml (P less than 0.0001) compared with the other groups showing mean values between 1.6 +/- 0.4 and 1.8 +/- 0.7 ng/ml. FPA was normal in one patient with HAPE, however. Severe AMS was accompanied by a significant decrease in arterial PO2 due to an increase in alveolar-arterial O2 difference, whereas arterial PCO2 did not change significantly. We conclude that activation of blood coagulation is not involved in the pathogenesis of AMS and the impairment of gas exchange in this disease. Fibrin generation occurring in HAPE is probably an epiphenomenon of edema formation.

Topics: Adult; Altitude Sickness; Arteries; Blood Coagulation; Blood Gas Analysis; Female; Fibrin; Humans; Hypoxia; Male; Pulmonary Edema

1987