Use of respiratory‐cardiovascular responses of rainbow trout (Salmo gairdneri) in identifying acute toxicity syndromes in fish: Part 1. pentachlorophenol, 2,4‐dinitrophenol, tricaine methanesulfonate and 1‐octanol

Abstract

An in vivo fish model was adapted to monitor respiratory-cardiovascular responses of spinally transected rainbow trout exposed to acutely toxic aqueous concentrations of two uncouplers of oxidative phosphorylation, pentachlorophenol (PCP) and 2,4-dinitrophenol (DNP), and two narcotics, tricaine methanesulfonate (MS-222) and 1-octanol. The most evident toxic response to the uncouplers was a rapid 150 to 200% increase in ventilation volume (V_G) and oxygen consumption (VO₂) over the entire survival period. This caused an initial increase in total arterial oxygen (T_aO₂) content of the blood, which then fell slowly as the tissues used more and more oxygen to generate ATP. Arterial blood pressure (BP_a) and other blood measurements did not change appreciably in response to PCP, yet DNP caused increases in hematocrit (Hct) and hemoglobin (Hb) and slight decreases in total arterial carbon dioxide (T_aCO₂) and arterial pH (pH_a). In contrast to the uncouplers, the response of the respiratory-cardiovascular system of trout to toxic levels of narcotics was a dramatic slowing of all respiratory-cardiovascular functions. While V_G and VO₂ decreased 40 to 50% from predose levels, oxygen utilization (U) increased 20 to 30%. Ventilation rate (VR) declined initially and then increased slowly until death occurred, but remained within the control range. As respiration declined T_aCO₂ significantly decreased, as did pH_a. In response to hypoxia, Hct increased substantially, and Hb increased slightly only in the 1-octanol exposure. A rapid 40 to 50% drop in heart rate (reflex bradycardia) was also observed. The final phase of toxicity caused by both uncouplers and narcotics appeared to eventually produce acute tissue hypoxia, with a generalized loss of respiratory-cardiovascular coordination, and finally respiratory paralysis. Individual principal component analyses of the cardiovascular-respiratory responses of fish exposed to the first two principal components explained 68 to 76% of the variation in the 18 parameters analyzed. A two-dimensional diagram of the first two principal components illustrated this multivariate response and the increased variability in the responses of exposed fish as compared with control fish. The general sets of responses described for these two fish acute toxicity syndromes have provided the initial information necessary to group similar responses caused by other chemicals into a fish uncoupler syndrome, a fish narcosis syndrome or some new syndrome.