6-ketoprostaglandin-f1-alpha and Altitude-Sickness

To study the effect of inhaled nitrogen monoxidum (NO) on endothelium-derived angiokinetic factors including NO, endothelin (ET), thromboxane B(2) (TXB(2)) and 6-keto-prostaglandin F(1a) (6-Keto-PGF(1a)) in patients with acute high altitude disease.. Forty-seven patients with acute high altitude disease were selected and divided into two groups randomly: twenty-three cases as a routine medical treatment group, for which oxygen, aminophylline, dexamethasone and furosemide were used, while 24 cases as a NO treatment group, for which only inhalation of 0.001% NO gas with air balanced in plateau (altitude 3658 m), were given twice daily (AM and PM each for an hour). The level of serum NO, ET, TXB(2) and 6-Keto-PGF(1a) were measured, and the changes of clinical symptoms were scored using the Lake Louise acute high altitude disease scoring.. In the two groups, the level of ET [(78 +/- 8) and (69 +/- 5) ng/L], TXB(2) [(87 +/- 13) and (73 +/- 8) ng/L], ET/NO [(26.7 +/- 1.5) x 10(3) and (21.8 +/- 1.1) x 10(3)], TXB(2)/6-Keto-PGF(1a) (0.84 +/- 0.36 and 0.58 +/- 0.11, clinical symptom score 2.4 +/- 1.6 and 1.8 +/- 1.3) after treatment were decreased significantly as compared to the levels of ET [(83 +/- 8) and (84 +/- 4) ng/L], TXB(2) [(102 +/- 16) and (103 +/- 13) ng/L], ET/NO [(35.0 +/- 2.7) x 10(3) and (36.3 +/- 3.1) x 10(3)], TXB(2)/6-Keto-PGF(1a) (1.28 +/- 0.38 and 1.24 +/- 0.28), clinical symptom score (4.4 +/- 2.3 and 4.4 +/- 2.0) before treatment. After treatment, the level of NO [(2880 +/- 537) and (3167 +/- 192) microg/L] and 6-Keto-PGF(1a) [(122 +/- 46) and (128 +/- 15) ng/L] were significantly higher than the level of NO [(2372 +/- 144) and (2313 +/- 188) microg/L] and 6-Keto-PGF(1a) [(86 +/- 28) and (86 +/- 13) ng/L] before treatment.. Inhaled NO is an effective treatment for high altitude disease in plateau, probably by modulating the angiokinetic factors.

Topics: 6-Ketoprostaglandin F1 alpha; Administration, Inhalation; Adolescent; Altitude Sickness; Endothelins; Endothelium; Humans; Male; Nitric Oxide; Thromboxane B2; Young Adult

To verify the presence of the constitutional abnormality implicated in the pathogenesis of high-altitude pulmonary edema (HAPE), we evaluated the hemodynamic responses to hypoxia, hypobaria, and exercise in HAPE-susceptible subjects (HAPE-S). HAPE-S were five males with a history of HAPE. Five healthy volunteers who had repeated experiences of mountain climbing without any history of altitude-related problems served as controls. HAPE-S showed much greater increase in pulmonary vascular resistance index (PVRI) than the control subjects, resulting in a much higher level of pulmonary arterial pressure (Ppa), under both acute hypoxia of 15% O2 (Ppa = 29.0 +/- 2.8 vs. 17.8 +/- 0.3 Torr, P less than 0.05) and acute hypobaria of 515 Torr (32.3 +/- 2.8 vs. 19.1 +/- 0.8 Torr, P less than 0.05). Also, PVRI in HAPE-S exhibited a tendency to increase even during light exercise with supine bicycle ergometer (50 W), whereas PVRI in the control subjects significantly decreased, so that HAPE-S showed a greater increase in Ppa (delta Ppa = 16.0 +/- 1.5 vs. 4.9 +/- 1.1 Torr, P less than 0.001) and a greater decrease in arterial oxygen tension (17.8 +/- 4.7 vs. 5.6 +/- 1.7 Torr, P less than 0.05). We thus conclude that HAPE-S have a constitutional abnormality, which can be evaluated at low altitude, in the pulmonary circulatory responses to possible causative factors of HAPE such as hypoxia, hypobaria, and exercise.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Altitude Sickness; Atmospheric Pressure; Atrial Natriuretic Factor; Blood Gas Analysis; Disease Susceptibility; Hemodynamics; Humans; Hypoxia; Male; Physical Exertion; Pulmonary Edema; Thromboxane B2