EFFECTS OF ACUTE TEMPERATURE-CHANGE, INVIVO AND INVITRO, ON THE ACID-BASE STATUS OF BLOOD FROM YELLOWFIN TUNA (THUNNUS-ALBACARES)

In most fishes, blood acid - base regulation following a temperature change involves active adjustments of gill ion-exchange rates which take hours or days to complete. Previous studies have shown that isolated blood from skipjack tuna, Katsuwonus pelamis, and albacore, Thunnus alalunga, had rates of pH change with temperature (in the open system) equivalent to those necessary to retain net protein charge in vivo (almost-equal-to -0.016-DELTA-pH . degrees-C-1). It was postulated that this is due to protons leaving the hemoglobin combining with plasma bicarbonate (HCO3-), which is removed as gaseous CO2, and that this ability evolved so that tunas need not adjust gill ion-exchange rates to regulate blood pH appropriately following ambient temperature changes. We reexamined this phenomenon using blood and separated plasma from yellowfin tuna, Thunnus albacares. Unlike previous studies, our CO2 levels (0.5 and 1.5 % CO2) span those seen in yellowfin tuna arterial and venous blood. Various bicarbonate concentrations ([HCO3-]) were obtained by collecting blood from fully rested as well as vigorously exercised fish. We use our in vitro data to calculate basic physiochemical parameters for yellowfin tuna blood: nonbicarbonate buffering (beta), the apparent first dissociation constant of carbonic acid (pK(app)), and CO2 Solubility (alpha-CO2). We also determined the effects of acute temperature change on arterial pH, [HCO3-], and partial pressures of O2 and CO2 in vivo. The pH shift of yellowfin tuna blood subjected to a closed-system temperature change did not differ from previous studies of other teleosts (almost-equal-to -0.016-DELTA-pH . degrees-C-1). The pH shift in blood subjected to open-system temperature change was Pco2 dependent and lower than that in skipjack tuna or albacore blood in vitro, but identical with that seen in yellowfin tuna blood in vivo. However, pH adjustments in vivo were caused by changes in both [HCO3-] and Pco2. The exact mechanisms responsible for these changes remain to be elucidated.