Increased ventricular stiffness and decreased cardiac function in Atlantic cod (Gadus morhua) at high temperatures

2013 ◽  
Vol 305 (8) ◽  
pp. R864-R876 ◽  
Author(s):  
Douglas A. Syme ◽  
A. Kurt Gamperl ◽  
Gordon W. Nash ◽  
Kenneth J. Rodnick

We employed the work loop method to study the ability of ventricular and atrial trabeculae from Atlantic cod to sustain power production during repeated contractions at acclimation temperatures (10°C) and when acutely warmed (20°C). Oxygen tension (Po2) was lowered from 450 to 34% air saturation to augment the thermal stress. Preparations worked under conditions simulating either a large stroke volume (35 contractions/min rate, 8–12% muscle strain) or a high heart rate (70 contractions/min, 2–4% strain), with power initially equal under both conditions. The effect of declining Po2 on power was similar under both conditions but was temperature and tissue dependent. In ventricular trabeculae at 10°C (and atria at 20°C), shortening power declined across the full range of Po2 studied, whereas the power required to lengthen the muscle was unaffected. Conversely, in ventricular trabeculae at 20°C, there was no decline in shortening power but an increase in lengthening power when Po2 fell below 100% air saturation. Finally, when ventricular trabeculae were paced at rates of up to 115 contractions/min at 20°C (vs. the maximum of 70 contractions/min in vivo), they showed marked increases in both shortening and lengthening power. Our results suggest that although elevated heart rates may not impair ventricular power as they commonly do isometric force, limited atrial power and the increased work required to expand the ventricle during diastole may compromise ventricular filling and hence, stroke volume in Atlantic cod at warm temperatures. Neither large strains nor high contraction rates convey an apparent advantage in circumventing this.

1988 ◽  
Vol 137 (1) ◽  
pp. 287-301 ◽  
Author(s):  
M. Axelsson

The nervous regulation of heart rate and stroke volume in the Atlantic cod Gadus morhua was investigated both in vivo, during rest and exercise, and in vitro. The cholinergic and adrenergic influences on the heart were estimated in experiments with injections of atropine and sotalol. At rest the cholinergic and adrenergic tonus on the heart were 38% and 21%, respectively (ratio 1.81:1). At the end of an exercise period, the cholinergic tonus had decreased to 15% but the adrenergic tonus had increased to 28% (ratio 0.54:1). The results suggest that variation of the cholinergic tonus on the heart is a major factor in the regulation of the heart rate. In one group of fish, cardiac output was also measured, allowing calculation of stroke volume. Cardiac output increased significantly during exercise, and this effect persisted in the presence of both atropine and sotalol, although the increase in heart rate was reduced or abolished. The persisting increase in cardiac output during exercise is due to an increase in stroke volume, reflecting a Starling relationship. In the presence of the adrenergic neurone-blocking agent bretylium, a positive inotropic effect on isolated, paced atrial and ventricular strips was observed. In the atrial preparations the effect persisted after 24 h. The effect was prevented by pretreatment with sotalol or cocaine, but potentiated by phentolamine pretreatment. This shows that bretylium exerts its neurone-blocking action after being taken up into the adrenergic nerves, and suggests that the positive inotropic effect of bretylium observed in vivo is due to release of endogenous catecholamines. The concentration-response curves for adrenaline on isolated spontaneously beating atrial preparations showed that the concentrations of catecholamines necessary to produce appreciable effects on the heart are higher than the concentrations found in cod plasma during ‘stress’ situations (handling and exhaustive swimming).


1994 ◽  
Vol 192 (1) ◽  
pp. 253-267 ◽  
Author(s):  
M Berenbrink ◽  
C Bridges

The effects of catecholamines on the pH and the cellular ion and water content were investigated in red blood cells from the Atlantic cod (Gadus morhua). Noradrenaline induced a rapid decrease in the extracellular pH (pHe) of red blood cells suspended in a CO2/bicarbonate or in a CO2/bicarbonate-free buffer system. The noradrenaline-induced changes in pHe were a saturable function of the external sodium ion concentration and were inhibited by amiloride but not by DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid, final concentration of both 10(-4) mol l-1). The catecholamine-induced extracellular acidification was accompanied by an intracellular alkalization and protons were moved from their electrochemical equilibrium. Proton extrusion was associated with an increase in the red blood cell sodium and chloride concentrations. In the presence of DIDS, the chloride movements were blocked and the net proton efflux under these conditions matched the net sodium influx. The results strongly suggested the activation of a sodium/proton exchanger by catecholamines in the red blood cells of the Atlantic cod. The red blood cell receptor affinity for adrenaline was three times higher than that for noradrenaline. Comparison with data in the literature for in vivo catecholamine concentrations indicated that adrenaline was more effective than noradrenaline in activating the red blood cell sodium/proton exchanger in the Atlantic cod in vivo.


1988 ◽  
Vol 140 (1) ◽  
pp. 171-186 ◽  
Author(s):  
KRISTINA SUNDELL ◽  
BJÖRN THRANDUR BJÖRNSSON

An in vitro technique for perfusion of the intestinal vasculature and lumen was developed and used to measure calcium (Ca2+) fluxes across the intestinal mucosa of the marine teleost, the Atlantic cod (Gadus morhua). Saturable and nonsaturable components of the calcium influx and efflux were determined. The calcium influx had one passive component and one saturable component, following Michaelis-Menten kinetics with Km = 8.41mmoll−1 and Vmax = 0.604μmol Ca2+ kg−1 h−1. At physiological Ca2+ concentrations in the vascular ([Ca2+] = l.9mmoll−1) and luminal ([Ca2+] =14.9mmoll−1) perfusion fluids, the saturable component amounted to 60% of the Ca2+ influx. The high-affinity Ca2+-ATPase inhibitor chlorpromazine (CP, 10−4moll−1) antagonized 45% of the Ca2+ influx. The Ca2+ efflux across the intestinal mucosa of the cod was a saturable process, following Michaelis-Menten kinetics with Km =6.15mmoll−1 and Vmax =3.79μmol Ca2+ kg−1h−1, but insensitive to CP (l0−5moll−1). The Ca2+ efflux was l.22μumol Ca2+ kg−1 h−1, representing about 20% of the total calcium excretion and about 50% of the extrarenal excretion of the Atlantic cod in vivo.


Vaccines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 34
Author(s):  
Verena Mertes ◽  
Alexander Kashulin Bekkelund ◽  
Leidy Lagos ◽  
Elia Ciani ◽  
Duncan Colquhoun ◽  
...  

Francisellosis in fish is caused by the facultative intracellular Gram-negative bacterial pathogens Francisella noatunensis ssp. noatunensis and Francisella orientalis. The disease is affecting both farmed and wild fish worldwide and no commercial vaccines are currently available. In this study, we tested isolated membrane vesicles (MVs) as possible vaccine candidates based on previous trials in zebrafish (Danio rerio) indicating promising vaccine efficacy. Here, the MV vaccine-candidates were tested in their natural hosts, Atlantic cod (Gadus morhua L.) and Nile tilapia (Oreochromis niloticus). Injection of MVs did not display any toxicity or other negative influence on the fish and gene expression analysis indicated an influence on the host immune response. However, unlike in other tested fish species, a protective immunity following vaccine application and immunization period could not be detected in the Atlantic cod or tilapia. Further in vivo studies are required to achieve a better understanding of the development of immunological memory in different fish species.


1991 ◽  
Vol 155 (1) ◽  
pp. 549-566 ◽  
Author(s):  
STEVE F. PERRY ◽  
REGINA FRITSCHE ◽  
RICHARD KINKEAD ◽  
STEFAN NILSSON

We have characterized the elevation of circulating catecholamines in the intact Atlantic cod (Gadus morhua) during graded acute (30 min) hypoxia. The potential mechanisms contributing to the mobilization of catecholamines during hypoxia were then assessed in vivo using nerve sectioning and pharmacological techniques and in situ using a perfused head kidney preparation. Pre-branchial plasma adrenaline concentrations were significantly elevated at all levels of aquatic hypoxia utilised [water Po2 (PWO2) = 10 kPa (75 mmHg), 7.3kPa (55 mmHg) or 5.3 kPa (40 mmHg)], whereas noradrenaline levels did not increase significantly in these particular experiments in which PWWOWO2 was lowered gradually over a 30 min period. All subsequent experiments were performed using a more rapid induction of hypoxia to reach a final PWWOWO2 of 5.3 kPa within the first 57–10 min of exposure. Blood withdrawn from pre-branchial (ventral aortic) and post-branchial (dorsal aortic) cannulae after 30 min revealed pronounced reductions in POO2 and O2 content (CO2) as well as elevated pH. These data support the notion that blood acidosis is not a prerequisite for catecholamine mobilization during hypoxia. Bilateral sectioning of spinal nerves 17-4 innervating the head kidney prevented the elevation of noradrenaline during rapidly induced hypoxia, but had no effect on the rise in plasma adrenaline concentration. After each experiment, fish were exposed to air for 3 min to induce severe stress. Plasma catecholamine levels were significantly reduced during stress, suggesting that the sectioning of the spinal nerves to the head kidney was indeed effective. These results indicated that mechanisms other than neural stimulation of head kidney chromaffin tissue were contributing to the rise in plasma adrenaline level during hypoxia. Neuronal overflow into the circulation, however, was an unlikely possibility since the increase of adrenaline could not be prevented by treating denervated fish with bretylium (an inhibitor of catecholamine release from adrenergic nerve terminals). These data suggested a local direct stimulatory effect of blood hypoxaemia on adrenaline release from chromaffin tissue. This hypothesis was confirmed using a blood-perfused head kidney preparation in which hypoxaemia markedly stimulated adrenaline overflow into the effluent blood. Further experiments using a Ringer-perfused head kidney preparation were designed to test the hypothesis that blood catecholamine levels in vivo are, in part, controlled by the concentration of catecholamines in the blood entering the head kidney. The results show conclusively that overflow of a particular catecholamine during cholinergic stimulation of the head kidney is controlled independently by the inflowing concentration of that catecholamine. We suggest that this mechanism of ‘auto-inhibition’ of catecholamine overflow is a functional negative feedback mechanism involved in the control of plasma catecholamine levels in the cod.


1985 ◽  
Vol 117 (1) ◽  
pp. 335-347 ◽  
Author(s):  
D. G. Smith ◽  
S. Nilsson ◽  
I. Wahlqvist ◽  
B. M. Eriksson

Dorsal (PDA) and ventral aortic blood pressure (PVA) and heart rate (HR) were measured in conscious resting cod, Gadus morhua L., which has been allowed 24 h recovery from surgery. Plasma adrenalin and nonadrenalin concentrations in these fish were 3.4 and 2.2 nmoll-1 respectively, and thus lower than previously reported values from partially recovered cod. Twenty-four hours after treatment with the adrenergic neurone blocking agent bretylium, PDA was significantly reduced by 17% compared to sham-injected controls, although PVA and heart rate were unaltered. Subsequent alpha-adrenoceptor blockade by phentolamine produced no further fall in PDA and no changes in PVA or HR, provided a 5-h period was allowed to overcome the acute toxic side effects of phentolamine. The effectiveness of the bretylium or phentolamine blockade was confirmed by noting the absence of any vasoconstrictor response during sympathetic nerve stimulation in perfused tails from fish used in the in vivo experiments. Bretylium had no significant effect on the sensitivity of the isolated coeliac artery to adrenalin, but effectively blocked the adrenergic innervation of this artery or the vasculature of the tail. Evidence for a non-selective blockade of non-adrenergic nerves to the heart was also obtained. It is concluded that the adrenergic tonus affecting the dorsal aortic blood pressure in resting cod that have recovered for 24 h following surgery is due solely to an adrenergic nervous tone.


2012 ◽  
Vol 109 (6) ◽  
pp. 1071-1081 ◽  
Author(s):  
Øystein Sæle ◽  
Andreas Nordgreen ◽  
Pål A. Olsvik ◽  
Jan I. Hjelle ◽  
Torstein Harboe ◽  
...  

We have previously described that fish larvae absorb a larger fraction of dietary monoacylglycerol than TAG. To investigate how dietary hydrolysed lipids affect a vertebrate at early life stages over time, we fed Atlantic cod (Gadus morhua) larvae six diets with different degrees of hydrolysed lipids for 30 d. The different diets had no effect on growth, but there was a positive correlation between the level of hydrolysed lipids in the diets and mortality. Important genes in lipid metabolism, such as PPAR, farnesoid X receptor (FXR) and stearoyl-CoA desaturase (SCD), were regulated by the different diets. Genes involved in the oxidative stress response did not respond to the increased lipid hydrolysation in the diets. However, enterocyte damage was observed in animals fed diets with 2·7 % NEFA (diet 3) or more. It is thus possible that mortality was due to infections and/or osmotic stress due to the exposure of the subepithelial tissue. In contrast to earlier experiments showing a positive effect of dietary hydrolysed lipids, we have demonstrated a toxic effect of dietary NEFA on Atlantic cod larvae. Toxicity is not acute but needs time to accumulate.


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