Adaptive respiratory responses of trout to acute hypoxia. III. Ion movements and pH changes in the red blood cell.
In the preceding paper acute hypoxia was shown to elicit within minutes an increase in the blood O2 affinity. From the present data it appears that this rapid change in blood P50 value can be ascribed to an important alkalization of the red blood cell despite a simultaneous decrease in extracellular pH (pHe). The intracellular alkalization is only partially due to beta-adrenergic stimulation of Na/H exchange, deoxygenation of hemoglobin and the rapid decrease of PaCO2 due to hyperventilation being involved in this process via the chloride shift. This high value of intraerythrocytic pH (pHi) is then maintained practically constant throughout the time the fish is kept in hypoxia despite wide changes of external pH. The blocking of pHi accounted for the constant O2 content observed during hypoxia. The uncoupling of pHi from pHe, which occurs at the onset of hypoxia, is still unexplained: for instance, it is not due to inhibition of the anion exchanger responsible for the passive distribution of H+ across the red cell membrane. A general scheme of all the mechanisms involved in the emergency adaptive response to acute hypoxia is presented.
D000818:Animals; D002245:Carbon Dioxide / Q000097:blood; D002712:Chlorides / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism*; D006454:Hemoglobins / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007474:Ion Exchange; D010100:Oxygen / Q000097:blood / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D012487:Salmonidae / Q000502:physiology*; D012964:Sodium / Q000378:metabolism; D014337:Trout / Q000097:blood / Q000502:physiology*
D002712:Chlorides; D006454:Hemoglobins; D002245:Carbon Dioxide; D012964:Sodium; D011188:Potassium; D010100:Oxygen