[The role of the prostaglandin system in the cardioprotective effect of adaptation to hypoxia in stress].

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.