Rainbow trout,Oncorhynchus mykiss, were exercise-trained for 18 hours per day over 28 days at water velocities up to 60% of their measured Ucrit. Anin situ perfused heart preparation was used to compare maximum cardiac performance between control and trained fish. Trained fish had a larger stroke volume at a given filling pressure, as well as an 18% higher cardiac output and a 25% greater maximum power output. These observations indicate that exercise training in rainbow trout improved maximum cardiac performance. Adrenaline produced positive inotropic and chronotropic effects on the perfused heart, but exercise training did not alter these stimulatory effects. Maximal activities of citrate synthase (CS), B-hydroxyacyl CoA dehydrogenase (HOAD), glutamate dehydrogenase (GDH) and carnitine palmitoyl transferase (CPT) were measured in cardiac and skeletal muscles. CS, HOAD and GDH increased in red and white skeletal muscle as a result of training. Training also increased GDH activity in the endocardium and epicardium, and increased HOAD in the epicardium. While the training regime did not result in a statistically significant increase in Ucrit and produced a decrease in the condition factor of the fish, other training effects were clearly evident. Furthermore, significant correlations were observed between Ucrit and the maximal activities of GDH and HOAD.

Rainbow trout, Oncorhynchus mykiss, were exercise trained for 28–52 days. Trained fish were 13% larger and swam 12% faster in an aerobic swimming test. Training induced cardiac growth that was isometric with body growth, since ventricle mass relative to body mass was constant. The proportions of compact and spongy myocardia in the ventricle were also unchanged by training. Trained fish had significantly higher levels of citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase in both compact and spongy myocardium. Ligation of a 0.5- to 1.0-cm section of the coronary artery produced only a temporary interruption of coronary flow to the compact myocardium because new vessels grew around the ligation site in the majority of fish during the 28- to 52-day experiment. Nonetheless, coronary ligation resulted in a significantly smaller (17%) proportion of compact myocardium with lower levels of citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase. Exercise-induced increases in the levels of these enzymes in the compact myocardium were prevented by coronary ligation. The decrease of enzymes in the compact myocardium as a result of coronary ligation was compensated for by a 30% increase in the levels of the aerobic enzymes citrate synthase and β-hydroxyacyl CoA dehydrogenase and a 32% increase in the mass of spongy myocardium. As a result of these compensations and coronary regrowth, chronic coronary ligation did not affect maximum prolonged swimming speed. These experiments clearly reveal that cardiac plasticity allows compensatory changes that are necessary for the heart to maintain adequate oxygen delivery to exercising skeletal muscle. The compensatory changes were isometric increases in heart mass or proportionately larger increases in heart mass and compact tissue if the coronary artery was ligated and an increase in metabolic enzymes associated with ATP generation, namely, citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase.

No abstract

The toxicity of Garlon4, the ethylene glycol butyl ether ester formulation of the herbicide tryclopyr, to juvenile coho salmon (Oncorhynchus kisutch) was investigated at several lethal and sublethal concentrations. Fish behavior, random activity and oxygen uptake were monitored. Coho salmon exhibited three distinct responses related to concentration and duration of exposure: (1) at concentrations greater than 0.56 mg/L fish were initially lethargic, then regressed to a highly distressed condition characterized by elevated oxygen uptake and finally death, (2) at 0.32-0.43 mg/L fish were lethargic throughout the exposure period with reduced oxygen uptake, and (3) at concentrations less than or equal to 0.10 mg/L fish were hypersensitive to stimuli, exhibiting elevated activity and oxygen uptake levels during photoperiod transitions. Whole body residue analysis showed that uptake of the ester and subsequent hydrolysis to the acid form in the fish was rapid, with significant accumulation of the acid in the tissues. This suggests that some threshold tissue concentrations were associated with the observed results. For juvenile coho salmon the 96-hr LC50 of Garlon4 was 0.84 mg/L.

This study surveyed and compared vasoactive responses of isolated coronary vessels from steelhead trout (Oncorhynchus mykiss), rainbow trout (also O. mykiss), and spiny dogfish (Squalus acanthias). The purpose of the investigation was twofold: to identify vasoactive controls that were possibly mediated by the vascular endothelium and to highlight the possible consequences on vasoactivity of the coronary lesions known to be present in the main coronary of salmonids but not dogfish. The test substances included acetylcholine, adenosine, adenosine triphosphate, adenosine diphosphate, serotonin, thrombin, bradykinin, prostaglandin F2α, prostaglandin I2, prostaglandin E2, and the fatty acids arachidonic acid, docosahexaenoic acid, and eicosapentaenoic acid. Acetylcholine, adenosine, adenosine triphosphate, adenosine diphosphate and prostaglandin F2α typically produced contractions. Use of endothelial removal techniques and antagonists failed to reveal any relaxations that might involve the endothelium. Thrombin and bradykinin had no vasoactivity. Serotonin, prostaglandin I2, and prostaglandin E2 produced relaxations that were not mediated by the endothelium. The powerful relaxations observed with prostaglandin I2 and prostaglandin E2 and the powerful contractions observed with prostaglandin F2α suggest a major role of prostanoids in coronary vasoactivity in fish. These prostanoid-mediated mechanisms, in addition to the previously demonstrated powerful contractions with endothelin-1, point to an important role for the endothelium. No major qualitative or quantitative differences in vasoactivity could be related to differences in coronary lesion severity.