The pathophysiology of chloramine-T on rainbow trout gills.

Title: The pathophysiology of chloramine-T on rainbow trout gills.
Authors: Powell, Mark D.
Date: 1997
Abstract: The goal of this thesis was to examine the pathophysiological effects of chloramine-T exposure on the respiratory, acid-base and ionoregulatory physiology of the rainbow trout gill. In particular, chloramine-T was used as a tool to probe the fundamental physiological processes of gas transfer, acid-base and ion regulation in response to branchial irritation. Exposure of rainbow trout (Oncorhynchus mykiss) to therapeutic and subtherapeutic concentrations of chloramine-T (9 mg.L$\sp{-1}$ and 2 mg.L$\sp{-1}$, respectively) caused acute respiratory and acid-base disturbances. These consisted of an increase in ventilation frequency and arterial blood PCO$\sb2$ (PaCO$\sb2$); arterial PO$\sb2$ (PaO$\sb2$) was unaffected. Exposure of fish to chloramine-T under hyperoxic and moderately hypoxic conditions suggested that CO$\sb2$ excretion was being impaired due to the secretion of mucus in response to irritation by hypochlorite. To verify that the apparent impediment to excretion was diffusional and not due to a reduced functional surface area for gas exchange, direct measurements of cardiac output, O$\sb2$ uptake, CO$\sb2$ excretion, dorsal and ventral aortic blood pressures were made. There were no changes in dorsal or ventral aortic pressures or in branchial or systemic vascular resistance. The perfusion convection requirement for CO$\sb2$, but not O$\sb2$, increased during exposure to chloramine-T even though there were consistent increases in cardiac output. Thus a greater blood flow than was achieved would be required to excrete an equivalent amount of CO$\sb2$ during chloramine-T exposure as under non-exposed (control) conditions. However, there was sufficient blood flow to maintain and even increase O$\sb2$ uptake. Repeated intermittent exposure of fish to chloramine-T resulted in a reduction in the thickness of the gill epithelial diffusion barrier and a mucous cell hyperlasia. The consequences of these morphological changes on gas exchange were assessed using a graded hypoxic challenge. There was no effect of chloramine-T treatment on oxygen uptake rates but fish which had been pre-treated with chloramine-T maintained their PaO$\sb2$ at higher levels at 70-80 mmHg water PO$\sb2$ compared with controls. PaCO$\sb2$ levels were not significantly different between control and experimental animals even though chloramine-T treated animals had higher ventilation frequencies under pre-hypoxic conditions. Acute acid-base disturbances during chloramine-T exposure consisted of a metabolic alkalosis superimposed over a respiratory acidosis. A study of the net and unidirectional ionic and acid-base fluxes across the gill confirmed that chloramine-T exposure caused a reduction in the uptake of acidic equivalents. Acute Na$\sp+$ and Cl$\sp-$ losses were also observed with chloramine-T exposure and were attributed to an increase in a transcellular rather than paracellular ionic efflux. Chloramine-T did not effect urine flow rate, glomerular filtration rate, renal Na$\sp+$ and Cl$\sp-$ effluxes or renal clearance of Na$\sp+$ and Cl$\sp-$. Exposure of soft-water acclimated fish to chloramine-T did not cause increased ionic losses, consistent with the theory of transcellular rather than paracellular ionic losses. Ionic losses in both normal tap water and artificial soft water acclimated trout were eliminated by the addition of 0.1% (w/v) NaCl to the water. (Abstract shortened by UMI.)
CollectionTh├Ęses, 1910 - 2010 // Theses, 1910 - 2010
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