Abstract
Buccal movements at the air-water interface causing surface water and air bubble inhalation ("surface breathing") and the resultant effects on blood O₂ transport have been quantified as a function of inspired water Po₂ in the goldfish, Carassius auratus. At 26 C, surface breathing occurred below a Po₂ of about 70 mmHg and increased to a peak of 180 surface breathing periods/h at Po₂ 20 mmHg. At this severe level of hypoxia, surface breathing resulted in a significant elevation of arterial Po₂ by 1.2 mmHg above that in control goldfish, which were not surface breathing. This very small rise in arterial Po₂ caused a sharp rise in arterial blood O₂ saturation from 16% to 33%, because of the high oxygen affinity ( ) and steep slope of the blood O₂ equilibrium curve. The net effect of surface breathing at the air-water interface during severe aquatic hypoxia is a 2.5 times increase in the arterial-venous O₂ saturation difference compared with strictly aquatic ventilation. Surface breathing with a nitrogen rather than air atmosphere significantly increased surface-breathing frequency and significantly decreased arterial blood oxygenation at a constant water Po₂. Surface breathing, which includes both "air gulping" and irrigation of the gills with the surface water layer, is thus demonstrated to have a significant respiratory function in the goldfish.