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Relationship between the arterial blood acid-base status and ventilation in the rainbow trout, Salmo gairdneri Janssen, Robert Gerrit


Studies were carried out to determine the influence of the change in the acid-base status of the blood on regulation of pH in relation to control of ventilation in the rainbow trout. By placing trout in ventilation (VG) boxes direct measurement of ventilation volume and rate could be made. Arterial blood was collected via chronically implanted catheters in the dorsal aorta; these catheters also allowing administration of the various acids and bases. The first series of experiments were designed to determine ventilatory responses to high ambient PCO₂ levels (hypercapnia) and the effect on regulation of arterial blood pH. Both short-term (up to 8 hours) and long-term (up to 72 hours) exposures were studied. PaO₂ levels remained saturated, or nearly so, throughout these experiments. The general response to high PCO₂ levels is an increase in the ventilatory stroke volume, this being mainly due to an increase in rather than VG. Compensation of ventilation during the sustained hypercapnia is slow, taking up to 3 days. Arterial H⁺ levels increased during CO₂ exposure, increasing from a control level of 11.8 ± 0.5 to 41.0 ± 3.5 nM/L within 5 minutes. There is a gradual decrease in arterial H⁺ concentration such that at 72 hours it is near normal. The time course of compensation for both VG and pHa coincide. The hypercapnia experiments indicate that in the face of an increase in ambient PCO₂ trout do not adjust the PCO₂, difference (ΔPCO₂ between arterial blood and water. PaCO₂ changes in proportion to the change in PICO₂ such that PaCO₂ is always about 2 mm Hg above ambient, demonstrating that ΔPCO₂ is not affected by changes in ventilation. The change in arterial blood pH is shown to be related to the transfer of CO₂ rather than by a transfer of H⁺ ions from water to blood. Arterial blood pH is regulated via adjustment of blood HCO⁻₃ levels, adjustment being in the order of 2 - 3 days. HCO⁻₃ can be regulated, or adjusted by either the kidney or the gills. The role of the kidney was shown to be minor in the adjustment of a NaHCO₃ induced alkalosis. Uptake of HCO⁻₃ is shown to occur when fish are placed in NaHCO₃ containing water, demonstrating the role of the gills in the amelioration of arterial blood pH. These observations are discussed in relation to a HCO⁻₃/Cl⁻ exchange. The ventilation volume is dependent on an increase in PaCO₂ and/or PICO₂ and not to pHa or pHI. A decrease in pHI, although causing a fall in pHa, has only a delayed effect on VG. The response in VG is transient. It is postulated that receptors are either adapting or are not located in the blood or water but in another compartment whose contents or properties change in proportion to ventilation. It is hypothesized that a chemosens.itive area may exist on the ventrolateral surface of the medulla as in mammals. Perfusion of the cranial cavity of trout with mock CSF, in which CO₂-HGO⁻₃ was altered, did not elicit respiratory responses. These experiments do not preclude the existence of medullary chemoreceptors. These results are consistent with the hypothesis that ventilation in trout is dependent on the CO₂ tension within the body or elsewhere and that blood pH levels are regulated via ionic exchange mechanisms at the gill surface, rather than by ion exchange at the kidney or by diffusive washout of gaseous CO₂ via ventilation.

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