ABSTRACT
In the tropical fresh water fish, Synbranchus marmoratus, transition from water breathing to air breathing, induced by reduction of oxygen partial pressure (
) in the environmental water below 16 mmHg, causes a considerable rise in the arterial partial pressure of carbon dioxide (
) from 5·6 to 26 mmHg on the average (half time of the rise between 2 and 6·5 h). The associated fall in arterial plasma pH by about 0·6 units is not compensated by an increase in plasma bicarbonate concentration, whereas the intracellular pH of white skeletal muscle and heart muscle is kept almost constant by elevation of the intracellular bicarbonate concentration. The additional bicarbonate is generated by intracellular non-bicarbonate buffering, and by net transfer into the intracellular space of bicarbonate formed by buffering in blood. Only a relatively small quantity of bicarbonate is taken up from environmental water.
This type of acid-base regulation, with almost complete intracellular pH compensation and only minor bicarbonate uptake (equivalent H+ release or OH− uptake) from water, is attributed to several factors. Probably the most important of these is the lack of continuous contact of the gills, which are the main site of ion transfer processes, with the environmental water during air breathing. Regardless of the mechanisms involved, this particular strategy of acid-base regulation provides a constant milieu for the intracellular structures and demonstrates the prevalence of intracellular over extracellular acid-base regulation.
The term ‘Bicarbonate transfer’ is descriptively used, although the mechanisms may involve transfer of OH− ions, or of H+ ions in opposite direction; they are indistinguishable by the methods used.
