thromboxane-a2 and Altitude-Sickness

What is the central question of this study? Is the expression of platelet-derived growth factor (PDGF) and thromboxane A2 (TXA2) elevated in chronic altitude patients, and are they related to thrombosis in chronic mountain sickness? What is the main finding and its importance? The expression of PDGF and TXA2 in both the bone marrow and the peripheral blood of patients with chronic mountain sickness is elevated, and they are considered to be correlated in the mechanism of thrombosis in the chronic mountain sickness.. The purpose of this study was to evaluate the expression of platelet-derived growth factor (PDGF) and thromboxane A2 (TXA2) along with platelet parameters and coagulation indices in chronic mountain sickness (CMS) patients and healthy individuals on the Qinghai-Tibet Plateau. The levels of PDGF and TXA2 were examined in 22 CMS patients (age, 52.77 ± 9.92 years, haemoglobin, 219 ± 13 g/l) and 25 healthy individuals (age, 47.80 ± 9.78 years, haemoglobin, 146 ± 18 g/l), and the association between platelet parameters and coagulation indices was investigated. Mean platelet volume and fibrinogen degradation product were higher in the CMS compared to the control group (10.58 ± 0.83 vs. 8.92 ± 1.61, 7.50 ± 2.15 vs. 4.40 ± 2.51), platelet count and plateletcrit were lower in the CMS compared to the control group (0.13 (0.80, 0.16) vs. 0.23 (0.18, 0.24), 109 ± 46 vs. 204 ± 86). The levels of PDGF and TXA2 in the bone marrow and peripheral blood of CMS patients were higher (P < 0.01) in comparison to the control group. The two factors had no statistically significant relationship with platelet parameters or coagulation indices (P > 0.159). According to the current findings, platelets in CMS patients were activated, resulting in aberrant coagulation and PDGF and TXA2 expression, which could be due to physiological adjustments to the plateau's high altitude. To summarize, PDGF and TXA2 levels in CMS patients were not correlated with coagulation or platelet parameters, implying that the mechanism behind their increased expression warrants additional investigation.

Topics: Adult; Altitude; Altitude Sickness; Chronic Disease; Hemoglobins; Humans; Middle Aged; Platelet-Derived Growth Factor; Thrombosis; Thromboxane A2

The adaptation to periodic altitude hypoxia is known to have cardioprotective and antiarrhythmic effects in stress-induced and ischemic lesions. The effects are assumed to be associated with the enhanced activity of the body's stress-limiting systems, including prostaglandins (PG). Wistar rats were adapted in a hypobaric chamber at an altitude of 4000 m for 6 hours during 40 days. The levels of myocardial and plasma PGE, PGE2 alpha, PGI2, thromboxane A2 were measured by radioimmunoassay and those of plasma catecholamines by enzyme radioassay. In the myocardium, the adaptation showed a 2-fold increase in PGE levels, the PGE/PGE2 alpha ratio and PGI2 levels rose by 70 and 73%, respectively, the PGI2/thromboxane A2 ratio remaining unchanged, while thromboxane A2 concentrations also rose. In adaptation, the levels of PGE and PGI2 was 78 and 60% higher, respectively. In restraint stress, myocardial and plasma PG levels proved to be substantially higher in adapted animals than in the controls, but stress-induced plasma catecholamine release, i.e. stress reaction, showed a 2-3-fold decrease that in the controls undergoing the same stress. The findings along with the data on the cytoprotective and vasodilating action of PGE and PGI2 suggest that enhanced activity of the myocardial and blood PG system is the important link in the mechanism responsible for the antistress impact of adaptation.

Topics: Adaptation, Physiological; Altitude Sickness; Animals; Catecholamines; Dinoprost; Disease Models, Animal; Epoprostenol; Male; Myocardium; Prostaglandins E; Rats; Rats, Wistar; Restraint, Physical; Stress, Psychological; Thromboxane A2