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A comparative study of the responses of the mast cell and coagulation systems to experimentally induced myocardial infarction in dogs that had been constantly hying at a medium altitude (1600 m above sea level) and those constantly hying at a low altitude (760 m) revealed less marked morphological and functional changes in these systems in the former ("mountain") dogs, which may be interpreted as an indication of their enhanced nonspecific resistance acquired as a result of long-term adaptation to conditions prevailing at medium altitudes.Studies in which the impact of various extremely adverse factors on the mast cell and coagulation systems was examined, have demonstrated that a relationship exists between the state of mast cells (MC) and alterations in the coagulation system [3,[9][10][11]. This prompted us to investigate the state and role of MC in pathological conditions involving coagulation disorders, given that MC are known Laboratory for the Study of Respiration and Blood Circulation, Institute of Physiology and Experimental Pathology at High Altitudes, Academy of Sciences of the Kyrgy'z Republic, Bishkek. {Presented by K. V. Sudakov, Member of the Russian Academy of Medical Sciences} to be producers of heparin and other biologically active substances [4,14]. There is evidence that MC can ensure equilibrium of the coagulation-anticoagulation system, for each cubic millimeter of wall of a large human blood vessel contains as many as 1000 to 8000 MC [13]. Patients with myocardial infarction hying in a plain region (around sea level) have been shown to have lowered blood levels of free heparin in conjunction with hypoplasia of MC and their reduced functional activity [7,8].The objective of the present study was to examine the impact of myocardial infarction on the functional state of MC in relation to changes in

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Vascular spasm, hypertrophy of cardiac muscle cells, and necrotic changes in the myocardial tissue of rats administered norepinephrine in incremental doses over 14 days were accompanied by a considerable activation of lipid peroxidation and a weakening of antioxidant defense during the first 7 days of exposure to this injurious agent. On day 14, despite the greatly increased load of norepinephrine, the concentrations of lipid peroxidation products and the activity of antioxidant enzymes deviated from their control values to a lesser extent than on day 7. A similar change was shown by the concentration of brain tissue phosphatidylinositol-4,5-diphosphate, a source of second messengers, suggesting that the phosphoinositide system of second messengers is involved in the mechanisms whereby the destructive effects of norepinephrine are mitigated.