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在对反复应激进行初步适应后对缺氧的超强抵抗力。

Superresistance against hypoxia after preliminary adaptation to repeated stress.

作者信息

Meerson F, Pozharov V, Minyailenko T

机构信息

Laboratory of Heart Pathophysiology, Russian Academy of Medical Sciences, Moscow.

出版信息

J Appl Physiol (1985). 1994 May;76(5):1856-61. doi: 10.1152/jappl.1994.76.5.1856.

DOI:10.1152/jappl.1994.76.5.1856
PMID:8063641
Abstract

The study investigated the influence of adaptation to stress on resistance to hypoxia. After rats were adaptated to moderate restraint stress, they were anesthetized and exposed to 6% O2. Adaptation increased tidal volume by 2.6-fold, lung and alveolar ventilation by 1.6- and 1.8-fold, respectively, and O2 consumption by 1.6-fold; limited lactate accumulation in the liver by 2-fold, in the heart by 34%, in the lung by 36%, and in the blood by 36%; and elevated pH. At the same time, preliminary adaptation to stress inhibited the hypoxic activation of lipolysis and peroxidation in all tissues. The concentration of lipid peroxides decreased after adaptation by 1.3- to 1.5-fold in different organs, whereas the content of free fatty acids diminished by 1.7- to 2.3-fold. Finally, after adaptation, mortality decreased under severe hypoxia by 6.5-fold. Thus, the data suggest that the cross-protective effect of adaptation was achieved by the economization of respiration and circulation, by marked augmentation in the ability of tissue to utilize blood O2, and by the limitation of processes that are able to damage tissue membranes, namely, acidosis, lipolysis, and lipid peroxidation.

摘要

该研究调查了应激适应对缺氧耐受性的影响。大鼠适应中度束缚应激后,进行麻醉并暴露于6%的氧气环境中。适应使潮气量增加了2.6倍,肺通气量和肺泡通气量分别增加了1.6倍和1.8倍,耗氧量增加了1.6倍;肝脏、心脏、肺和血液中乳酸积累分别受限2倍、34%、36%和36%;pH值升高。同时,预先适应应激抑制了所有组织中脂肪分解和过氧化的缺氧激活。适应后,不同器官中脂质过氧化物的浓度降低了1.3至1.5倍,而游离脂肪酸的含量减少了1.7至2.3倍。最后,适应后,严重缺氧条件下的死亡率降低了6.5倍。因此,数据表明,适应的交叉保护作用是通过呼吸和循环的节约、组织利用血液中氧气能力的显著增强以及对能够损害组织膜的过程(即酸中毒、脂肪分解和脂质过氧化)的限制来实现的。

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