The role of adrenergic stimulation in maintaining maximum cardiac performance in rainbow trout (Oncorhynchus mykiss) during hypoxia,hyperkalemia and acidosis at 10°C

Abstract

SUMMARY As rainbow trout approach exhaustion during prolonged exercise, they maintain maximum cardiac output despite the fact their venous blood, which bathes the heart, becomes hypoxic, acidotic and hyperkalemic. Because these factors are individually recognized to have detrimental inotropic and chronotropic effects on cardiac performance, we hypothesized that adrenergic stimulation is critical in maintaining maximum cardiac performance under these collectively adverse conditions in vivo. To test this hypothesis,maximum cardiac performance in the presence and absence of maximal adrenergic stimulation was assessed with in situ rainbow trout hearts using relevant hyperkalemic (5.0 mmol l–1 K+), acidotic(pH 7.5) and hypoxic challenges. With tonic adrenergic stimulation (5.0 nmol l–1 adrenaline), hearts produced only 44.8±14.6% of their normal maximum cardiac output when exposed under normoxic conditions (20 kPa) to the hyperkalemic, acidotic perfusate, indicating that in vivothere was no refuge from cardiac impairment even if venous blood was fully oxygenated. By contrast, maximum adrenergic stimulation (500 nmol l–1 adrenaline), fully protected maximum cardiac performance under hyperkalemic and acidotic conditions over a wide range of oxygen availability, from normoxia to 2.0 kPa, a venous oxygen tension close to routine values in vivo. Extending the level of hypoxia to 1.3 kPa resulted in a 43.6±2.8% decrease in maximum cardiac output, with hearts failing when tested at 1.0 kPa. Our results suggest that adrenergic stimulation of the trout heart is critical in maintaining maximum performance during prolonged swimming tests, and probably during all forms of exhaustive activity and recovery, when venous blood is hyperkalemic, acidotic and hypoxic.

Exceptional CO2Tolerance in White Sturgeon (Acipenser transmontanus) Is Associated with Protection of Maximum Cardiac Performance during Hypercapnia In Situ

“…An increase in Pco 2 to 8 kPa reduced Q max and PO max to a degree similar to that observed at 6 kPa but also resulted in arrhythmia without recovery in subsequent normocapnia. These data imply that cardiac damage, or at the very least temporary myocardial dysfunction (e.g., Hanson et al 2006), occurs at 8-kPa co 2 , a level of hypercarbia known to induce morbidity in vivo (D. W. Baker and C. J. Brauner, unpublished observations). ).…”

“…Maximum cardiac performance of white sturgeon heart has not been previously assessed in situ, but it would be expected to be lower than that of a pelagic predator such as rainbow trout. Relative to those of rainbow trout, white sturgeon hearts exhibited a 50% lower intrinsic f H (at 10ЊC; Arthur et al 1992;Hanson et al 2006), a 20%-40% lower Q max (Hanson et al 2006), and a 75% lower PO max (Hanson et al 2006). The lower power output of white sturgeon hearts (∼1.2-1.5 mW g ventricle Ϫ1 ) may reflect their limited athletic prowess.…”

“…The in situ heart preparation used in this study has been described in detail for different species, with a variety of minor modifications (Farrell et al 1983;Farrell and Milligan 1986;Hanson et al 2006Hanson et al , 2009. In brief, white sturgeon (300-1,300 g; relative ventricular weight ) were anesthe-0.096% ‫ע‬ 0.003% tized in buffered tricaine methane sulfonate (0.3 g L Ϫ1 of both MS-222 and NaHCO 3 ), weighed, and transferred to an operating table.…”

Atlantic cod (Gadus morhua L.) in situ cardiac performance at cold temperatures: long-term acclimation, acute thermal challenge and the role of adrenaline

“…Specifically, data on 10°C-acclimated Atlantic cod (Axelsson, 1988) suggest that adrenaline is not required for basal or maximum cardiac performance, whereas studies on several teleosts show that adrenergic sensitivity is a critical compensatory mechanism that enables the fish myocardium to maintain contractility during acute cold exposure (e.g. Franklin and Davie, 1992;Keen et al, 1993;Aho and Vornanen, 2001;Shiels et al, 2003;Galli et al, 2009), hypoxia and alterations in blood chemistry that are associated with intense exercise (Hanson et al, 2006). However, the apparent lack of myocardial responsiveness to adrenaline in cod may be due to the fact that only a single experimental temperature (10°C) has been examined to date.…”

Perinatal Hypoxia Induces Anterior Chamber Changes in the Eyes of Offspring Fish

“…Some previous studies have shown that certain important organs, including the brain [21,35] and cardiorespiratory system [18,19,36], have a contingent mechanism to combat hypoxia. However, these strategies did not seem to apply to the ocular system, which might predispose the eyes to developmental damage upon hypoxia.…”