Handa Takeshi

We investigated the effect of temperature on disk abalone Haliotis (Nordotis) discus discus hemolymph CO_2 solubility coefficient (αco_2) and the apparent dissociation constant of carbonic acid (pKapp). The disk abalone hemolymph was equilibrated with a standard CO_2 gas mixture between 10℃ and 20℃, to obtain expressions for αco_2 and pKapp as a function of temperature. The relationship between αco_2 and temperature (T) is expressed as follows： αco_2 = 74.005 - 1.2936 • T - 0.00944 • T^2. And the relationship between pKapp and temperature expressed as follows： pKapp = 6.4675 - 0.08682 • T + 0.003996 • T^2. In these equations, the parameter units are ℃ for T and µM/L/torr for αco_2. The non-bicarbonate buffer values (ꞵ_NB), obtained as a regression coefficient relating pH and [HCO_3^–], were 2.5 Slykes at 10℃, 2.2 Slykes at 15℃, and 3.4 Slykes at 20℃. These equations enable estimation of hemolymph αco_2 and pKapp between temperatures of 10℃ and 20℃.

We investigated the hemolymph oxygen and acid–base status of Akoya pearl oysters, Pinctada fucata martensii, exposed to hypoxic seawater to elucidate the acid–base balance. Akoya pearl oysters cannulated to the anterior aorta for hemolymph collection from the submerged animals showed oxygen and acid–base disturbance of the hemolymph during environmental hypoxia for 24 h (O_2 partial pressure in seawater, Pwo_2 8 torr). The hemolymph O_2 partial pressure (Po_2) decreased from 72.2 torr to 13.6 torr, pH decreased from 7.581 to 7.129, and CO_2 partial pressure (Pco_2) increased from 0.86 torr to 3.31 torr during hypoxia. The hemolymph total CO_2 concentration (Tco_2) and bicarbonate ion concentration ([HCO_3^–]) were 1.93–1.95 mM/L and 1.80–1.91 mM/L, respectively, and there was no statistically significant change between pre-hypoxia and hypoxia for 24 h. When normoxic seawater was resumed after the hypoxia, the hemolymph Po_2, pH, and Pco_2 returned to their initial levels for about 3 h, and hemolymph Tco_2 and [HCO_3^–] gradually increased. These results showed that Akoya pearl oysters undergo hypoxemia and respiratory acidosis in the hypoxic environments for 24 h (Pwo_2 8 torr). In post-hypoxia, most of the disturbances disappeared within 3–24 h, and the increase in hemolymph [HCO_3^–] which was a secondary change compensated for respiratory disturbance.

We investigated the hemolymph oxygen and acid–base status of akoya pearl oysters, Pinctada fucata martensii, exposed to air for a short time (4 h) to elucidate the acid–base balance and CO_2 dynamics. The hemolymph O_2 partial pressure (Po_2) in air-exposed akoya pearl oysters decreased from 88.7 torr (mean value) to 29.4 torr at 1 h, and the low Po_2 continued for the next 3 h during air exposure. The hemolymph pH decreased from 7.586 to 7.082 during air exposure for 1 h and reached 6.851 at 4 h. The hemolymph CO_2 partial pressure increased from 0.9 torr to 4.4 torr at 1 h and reached 7.3 torr after 4 h of air exposure. The hemolymph bicarbonate concentration and calcium ion concentration at 0 h (control) were 1.9 mM/L and 9.0 mM/L, respectively, and these properties did not significantly change during air exposure. From these results, it was determined that the akoya pearl oysters had hypoxemia caused by hypoventilation at an early phase of the short-term air exposure. The akoya pearl oysters inhibited the discharge of CO_2 by hypoventilation, and respiratory acidosis was caused due to the excessive accumulation of CO_2. Bicarbonate was not mobilized from the shell valve into the hemolymph during the short-term air exposure.

We investigated the oxygen and acid–base status of the densely lamellated oyster, Ostrea denselamellosa, during air exposure for 24 h. The hemolymph O_2 partial pressure decreased from 68.0 torr (mean value) to 52.1 torr during air exposure for 18 h, and reached 42.1 torr after 24 h. The hemolymph pH decreased from 7.579 to 6.798 at 18 h and to 6.361 at 24 h. The hemolymph CO_2 partial pressure increased from 1.30 torr to 40.9 torr at 24 h during air exposure. The hemolymph bicarbonate concentration increased from 1.36 mM/L to 2.81 mM/L at 24 h. The hemolymph calcium ion concentration increased from 8.2 mM/L to 10.9 mM/L at 24 h. From these results, it was revealed that the densely lamellated oysters caused a progressive hypoxemia by hypoventilation of the gill during air exposure. The densely lamellated oysters were inhibited from releasing CO_2 from the gill by hypoventilation, and respiratory acidosis was caused due to the accumulated CO_2. The densely lamellated oysters exposed to air for a long time developed metabolic acidosis due to anaerobic metabolism partially compensated with mobilized [HCO_3^–] from the shell valve.

We investigated the oxygen and acid–base status of the noble scallop Mimachlamys nobilis during air exposure for 24 h. The hemolymph of noble scallop was collected from the adductor muscle, and O_2 partial pressure (Po_2), pH, CO_2 partial pressure (Pco_2), and bicarbonate ion concentration ([HCO_3^–]) were examined during air exposure. Hemolymph Po_2 decreased from 69.5 torr (mean value) to 46.3 torr during air exposure for 6 h, and reached to 19.0 torr after 24 h. The hemolymph Po_2 of air-exposed noble scallops decreased gradually and caused progressive hypoxemia by hypoventilation of the ctenidium. Air-exposed noble scallops showed a reduction in pH and elevation of Pco_2 and [HCO_3^–] of the hemolymph. In air-exposed noble scallops, the hemolymph pH decreased from 7.460 to 7.045 at 6 h and to 6.348 at 24 h. The hemolymph Pco_2 increased from 1.30 torr to 5.05 torr at 6 h and to 56.6 torr at 24 h during air exposure. The [HCO_3^–] increased from 1.26 mM/L to 1.88 mM/L at 6 h and to 4.19 mM/L at 24 h. N32From these results, in the first 6 h of air exposure, noble scallops mainly underwent respiratory acidosis by excess accumulation of CO_2 due to hypoventilation. Meanwhile, after 24 h of air exposure, noble scallops showed mainly metabolic acidosis partially compensated by mobilized [HCO_3^–] from the shell.