Pak G D, Sverchkov V S, Danilevskaia T N, Trandafilova T P
Kosm Biol Aviakosm Med. 1988 Jan-Feb;22(1):49-53.
Acute experiments were carried out on 50 dogs to study the effect of epinephrine in hypoxic (N2 - 15 to 10% O2) or hypoxic-hypercapnic (N2 - 10%, O2 - 5% CO2) atmospheres. Epinephrine led to a maximum increase of blood coagulation and fibrinolysis in normoxic atmosphere. Hypoxia reduced the shift of most hemostasis parameters in response to epinephrine. However, in N2 - 10% O2 atmosphere the epinephrine-induced increase of blood coagulation was superimposed on initial hypoxic hypercoagulation and caused serious disorders in hemostasis. In hypoxic-hypercapnic atmosphere increase of blood coagulation in response to epinephrine was more than doubled when compared to that in hypoxic atmosphere, reaching control values. Nevertheless, after epinephrine administration the ratio of coagulatory, anticoagulatory and fibrinolytic activities was more beneficial in hypoxia-hypercapnia and the coagulation potential was lower than in hypoxic or normoxic atmospheres.
对50只狗进行了急性实验，以研究肾上腺素在低氧（氮气-15%至氧气-10%）或低氧高碳酸血症（氮气-10%，氧气-5%，二氧化碳）环境中的作用。在常氧环境中，肾上腺素导致血液凝固和纤维蛋白溶解的最大增加。低氧减少了大多数止血参数对肾上腺素的反应变化。然而，在氮气-10%氧气的环境中，肾上腺素诱导的血液凝固增加叠加在初始低氧高凝状态上，并导致止血严重紊乱。与低氧环境相比，在低氧高碳酸血症环境中，肾上腺素引起的血液凝固增加增加了一倍多，达到对照值。尽管如此，给予肾上腺素后，凝血、抗凝和纤维蛋白溶解活性的比率在低氧高碳酸血症中更有利，且凝血潜力低于低氧或常氧环境。
