Boutilier R G, Dobson G, Hoeger U, Randall D J
Department of Biology, Dalhousie University, Halifax, Nova Scotia, Canada.
Respir Physiol. 1988 Jan;71(1):69-82. doi: 10.1016/0034-5687(88)90116-8.
We have studied the mechanisms of acute hypoxia tolerance in rainbow trout (Salmo gairdneri). Fish held at 9 degrees C were exposed to various levels of hypoxia for 24 h. At an environmental PO2 of 30 Torr, the fish showed an initial plasma acidosis probably of metabolic origin which was subsequently offset such that blood pH returned to normal within about 4 h. Over this time period, red cell pH was maintained constant. Comparing the effects of different levels of hypoxia following 24 h exposure, oxygen consumption of the animal remained unchanged over a broad range of inspired oxygen tensions but declined by over 30% of normoxic values at inspired water PO2 levels of 80 Torr. This appeared to be a true metabolic depression because signs of increased anaerobic metabolism did not occur until there was a further reduction in water oxygen levels. Rainbow trout appear to be able to maintain a relatively high energy status in their white muscle during 24 h exposure to severe hypoxia (water PO2 = 30 Torr). As the level of hypoxia was intensified, there was a reduction in the oxygen gradient across the gills, probably facilitated in part by the release of catecholamines into the blood. The erythrocytic ATP: Hb4 molar ratios declined with increasing hypoxic stress as did the pH gradient between the erythrocyte and plasma. The overall effect was no change in Hb O2-affinity after 24 h exposure to severe hypoxia.
我们研究了虹鳟(Salmo gairdneri)急性耐缺氧的机制。将饲养在9摄氏度的鱼暴露于不同程度的缺氧环境中24小时。在环境氧分压为30托时,鱼最初表现出可能源于代谢的血浆酸中毒,随后这种酸中毒得到抵消,使得血液pH值在约4小时内恢复正常。在此期间,红细胞pH值保持恒定。比较24小时暴露于不同程度缺氧后的影响,动物的耗氧量在很宽的吸入氧分压范围内保持不变,但在吸入水氧分压为80托时,耗氧量比常氧值下降了超过30%。这似乎是一种真正的代谢抑制,因为直到水氧水平进一步降低,才出现无氧代谢增加的迹象。虹鳟在暴露于严重缺氧(水氧分压 = 30托)24小时期间,似乎能够在其白肌中维持相对较高的能量状态。随着缺氧程度的加剧,鳃上的氧梯度减小,这可能部分得益于儿茶酚胺释放到血液中。随着缺氧应激的增加,红细胞的ATP:Hb4摩尔比以及红细胞与血浆之间的pH梯度均下降。24小时暴露于严重缺氧后,血红蛋白与氧亲和力的总体效应没有变化。