The intercellular organization of the two muscular systems in the adult salmonid heart, the compact and the spongy myocardium

Stress and elevated cortisol levels are associated with pathological heart growth and cardiovascular disease in humans and other mammals. We recently established a link between heritable variation in post-stress cortisol production and cardiac growth in salmonid fish too. A conserved stimulatory effect of the otherwise catabolic steroid hormone cortisol is probably implied, but has to date not been established experimentally. Furthermore, whereas cardiac growth is associated with failure of the mammalian heart, pathological cardiac hypertrophy has not previously been described in fish. Here, we show that rainbow trout (Oncorhynchus mykiss) treated with cortisol in the diet for 45 days have enlarged hearts with lower maximum stroke volume and cardiac output. In accordance with impaired cardiac performance, overall circulatory oxygen-transporting capacity was diminished as indicated by reduced aerobic swimming performance. In contrast to the well-known adaptive/physiological heart growth observed in fish, cortisol-induced growth is maladaptive. Furthermore, the observed heart growth was associated with up-regulated signature genes of mammalian cardiac pathology, suggesting that signalling pathways mediating cortisol-induced cardiac remodelling in fish are conserved from fish to mammals. Altogether, we show that excessive cortisol can induce pathological cardiac remodelling. This is the first study to report and integrate the etiology, physiology and molecular biology of cortisol-induced pathological remodelling in fish.

Section: Chronic Cortisol Exposure Induces Cardiac Hypertrophy In Raimentioning

confidence: 99%

Bigger is not better: cortisol-induced cardiac growth and dysfunction in salmonids

Johansen

Sandblom

Skov

et al. 2017

“…One feature of the zebrafish heart that may play a role in compensating for the influence of low temperature on ventricle compliance is the compact myocardium. The compact myocardium is a layer of densely packed cells on the outside of the ventricle that helps to provide biomechanical support to the spongy myocardium (Hu et al, 2001;Pieperhoff et al, 2009). In this position it has the ability to influence the extension of the ventricle.…”

Section: Changes In Gross Morphology Of the Heartmentioning

confidence: 99%

Cold acclimation alters the connective tissue content of the zebrafish (Danio rerio) heart

Johnson

Turko

Klaiman

et al. 2014

Thermal acclimation can alter cardiac function and morphology in a number of fish species, but little is known about the regulation of these changes. The purpose of the present study was to determine how cold acclimation affects zebrafish (Danio rerio) cardiac morphology, collagen composition and connective tissue regulation. Heart volume, the thickness of the compact myocardium, collagen content and collagen fiber composition were compared between control (27°C) and cold-acclimated (20°C) zebrafish using serially sectioned hearts stained with Picrosirius Red. Collagen content and fiber composition of the pericardial membrane were also examined. Cold acclimation did not affect the volume of the contracted heart; however, there was a significant decrease in the thickness of the compact myocardium. There was also a decrease in the collagen content of the compact myocardium and in the amount of thick collagen fibers throughout the heart. Cold-acclimated zebrafish also increased expression of the gene transcript for matrix metalloproteinase 2, matrix metalloproteinase 9, tissue inhibitor of metalloproteinase 2 and collagen Type I α1. We propose that the reduction in the thickness of the compact myocardium as well as the change in collagen content may help to maintain the compliance of the ventricle as temperatures decrease. Together, these results clearly demonstrate that the zebrafish heart undergoes significant remodeling in response to cold acclimation.

“…Tilapia are hypoxia-tolerant cichlid fishes that inhabit environments that can experience regular bouts of hypoxia. Tilapia lack a coronary circulation (Pieperhoff et al, 2009), and they downregulate routine cardiac activity in hypoxia in vivo (SpeersRoesch et al, 2010). Speers-Roesch and colleagues showed that tilapia (Oreochromis hybrid: Oreochromis niloticus ϫ mossambicus ϫ hornorum) exposed to 8h at a water partial pressure of oxygen (P O2 ) of 1kPa decreased f H , cardiac output (Q) and PO by 50-60% (Speers-Roesch et al, 2010), and affirmed previous claims that bradycardia is an important component of cardiac hypoxia tolerance (Farrell, 2007;Farrell and Stecyk, 2007).…”

Section: Introductionmentioning

confidence: 99%

Exceptional cardiac anoxia tolerance in tilapia (Oreochromis hybrid)

Lague¹,

Speers‐Roesch

Richards

et al. 2012

SUMMARYAnoxic survival requires the matching of cardiac ATP supply (i.e. maximum glycolytic potential, MGP) and demand (i.e. cardiac power output, PO). We examined the idea that the previously observed in vivo downregulation of cardiac function during exposure to severe hypoxia in tilapia (Oreochromis hybrid) represents a physiological strategy to reduce routine PO to within the heartʼs MGP. The MGP of the ectothermic vertebrate heart has previously been suggested to be ~70nmol ATPs -1 NaCN) on cardiac performance in severe hypoxia were also examined. Under normoxic conditions, cardiac performance and myocardial oxygen consumption rate were comparable to those of other teleosts. The tilapia heart maintained a routine normoxic cardiac output (Q) and PO under all hypoxic conditions, a result that contrasts with the hypoxic cardiac downregulation previously observed in vivo under less severe conditions. Thus, we conclude that the in vivo downregulation of routine cardiac performance in hypoxia is not needed in tilapia to balance cardiac energy supply and demand. Indeed, the MGP of the tilapia heart proved to be quite exceptional. Measurements of myocardial lactate efflux during severe hypoxia were used to calculate the MGP of the tilapia heart. The MGP was estimated to be 172nmol ATPs , which is only 30% lower than the PO max observed with normoxia. Even with this MGP, the additional challenge of acidosis during severe hypoxia decreased maximum ATP turnover rate and PO max by 30% compared with severe hypoxia alone, suggesting that there are probably direct effects of acidosis on cardiac contractility. We conclude that the high maximum glycolytic ATP turnover rate and levels of PO, which exceed those measured in other ectothermic vertebrate hearts, probably convey a previously unreported anoxia tolerance of the tilapia heart, but a tolerance that may be tempered in vivo by the accumulation of acidotic waste during anoxia.