This thesis examines the branchial mechanisms utilized by freshwater fish to regulate internal acid-base status and presents a model to explain the underlying basis of the compensatory processes. Rainbow trout, Oncorhynchus mykiss, brown bullhead, Ictalurus nebulosus, and American eels, Anguilla rostrata, were examined under a variety of experimental treatments which induced both respiratory (hyperoxia, hypercapnia) and metabolic (post-hyperoxia, post-hypercapnia, HCl infusion, NaHCO$\sb3$ infusion) acid-base disturbances. Acid-base-regulation was achieved by appropriate adjustments of Na$\sp+$ and Cl$\sp-$ net fluxes across the gills which, in turn, were accomplished by variable contributions of three different branchial mechanisms; (i) morphological adjustments to the gill epithelium, (ii) changes in internal (H$\sp+,$ HCO$\sb3\sp-)$ and external (Na$\sp+,$ HCO$\sb3\sp-)$ substrate availability, and (iii) differential changes in Na$\sp+$ versus Cl$\sp-$ net fluxes through regulation of Cl$\sp-$ efflux. This thesis determined the variable contribution of each of these mechanisms to overall compensation of acid-base disturbances. In brown bullhead and trout, respiratory acidosis caused a reduction in chloride cell (CC) surface area whereas alkalosis was associated with increases in CC surface area. Increases in the density of microvilli displayed on the external surface of the PVC coupled with ultrastructural modifications during hypercapnic acidosis were associated with increases in Na$\sp+$ uptake $\rm(J\sb{in}\sp{Na+}).$ In addition to the effect that alterations in CC surface area have on the rate of Cl$\sp-$/HCO$\sb3\sp-$ exchange $\rm(J\sb{in}\sp{Cl-}),$ it was demonstrated that changes in the concentration of the internal counter-ion (HCO$\sb3\sp-)$ may alter the rates of acid-base compensation. When (HCO$\sb3\sp-$) is elevated, $\rm J\sb{max}\sp{Cl-}$ is elevated thereby increasing the capacity to excrete HCO$\sb3\sp-$ via the Cl$\sp-$/HCO$\sb3\sp-$ exchanger over and above those determined by CC morphology. This is an important mechanism to increase the rate of acid-base compensation during metabolic alkalosis. (Abstract shortened by UMI.)
| Identifer | oai:union.ndltd.org:uottawa.ca/oai:ruor.uottawa.ca:10393/6794 |
| Date | January 1993 |
| Creators | Goss, Gregory Gerard. |
| Contributors | Perry, Steve, |
| Publisher | University of Ottawa (Canada) |
| Source Sets | Université d’Ottawa |
| Detected Language | English |
| Type | Thesis |
| Format | 319 p. |
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