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Control of the function of the heart in teleost fish Bennion, Glenda Ruth


The purpose of this study was to elucidate some of the mechanisms involved in the control of the function of the fish heart. In vitro experiments were conducted to determine the effect of varying input pressure, temperature, and epinephrine concentration on the isolated, perfused, trout heart. In vivo experiments were conducted with chronically implanted flow probes to determine the effect of increased blood epinephrine levels on the activity of the heart of the lingcod. Five variables were measured to describe the activity of the isolated trout heart: rate, stroke volume, cardiac output, stroke work, and heart work per minute. Heart function curves were constructed showing the relationship between each of these variables and the input pressure at two levels of epinephrine, 0.1 ug/ml and 0.01 ug/ml, and at two temperatures, 6°C and 15°C. The isolated trout heart obeyed Starling's law, since the stroke work increased as the filling pressure, and thus the end diastolic fiber length, increased. Increased filling pressure also caused the heart rate to increase, probably due to a direct effect of pressure on the pacemaker cells. Increased temperature produced an increase in rate, which in turn decreased the filling time available between beats and so decreased the stroke volume. Cardiac output was not greatly affected by temperature changes. Low temperature appeared to have a direct inotropic effect on the heart as well; that is, greater stroke work was produced from a given end diastolic volume at low temperatures. Epinephrine had a pronounced inotropic effect at 15°C. The stroke volume, stroke work, cardiac output, and heart work per minute all increased with high epinephrine. The rate decreased, probably because the systolic emptying was so much more complete that a greater time interval between beats was needed to fill the heart. At 6°C the inotropic effect of low temperature masked the inotropic effect of epinephrine, so that high epinephrine produced no change in stroke work or stroke volume. A positive chronotropic effect was pronounced at this temperature. The cardiac output and heart work per minute increased with epinephrine as a result. The adrenergic receptors mediating the responses of the heart to epinephrine were of the β-type only. The responses were blocked by Inderal, a β-receptor blocking agent, but were unaffected by phenoxybenzamine, an ⍺-receptor blocking agent. Increased levels of epinephrine in the blood of the lingcod at 10° - 12°C produced an increase in the mean blood flow in the ventral aorta. The heart rate remained constant, thus the changes in mean blood flow were due to changes in stroke volume. These stroke volume changes could be produced by epinephrine acting on the heart directly via β-receptors in the myocardium or indirectly via changes produced in the rest of the circulatory system.

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