Effects of temperature and anoxia upon the performance of in situ perfused trout hearts

SUMMARYRecent in vivo experiments on Atlantic cod (Gadus morhua) acclimated to chronic hypoxia (6-12weeks at 10°C; PW O2~8 -9kPa) revealed a considerable decrease in the pumping capacity of the heart. To examine whether this diminished cardiac performance was due to the direct effects of chronic moderate hypoxia on the myocardium (as opposed to alterations in neural and/or hormonal control), we measured the resting and maximum in situ function of hearts from normoxia-and hypoxia-acclimated cod:(1) when initially perfused with oxygenated saline; (2) at the end of a 15min exposure to severe hypoxia (P O2~0 .6kPa); and (3) 30min after the hearts had been reperfused with oxygenated saline. Acclimation to hypoxia did not influence resting (basal) in situ cardiac performance during oxygenated or hypoxic conditions. However, it caused a decrease in maximum cardiac output (Q max ) under oxygenated conditions (from 49.5 to 40.3mlmin , yet, the hearts of hypoxiaacclimated fish were better able to sustain this level of Q under hypoxia, and the recovery of Q max (as compared with initial values under oxygenated conditions) was significantly improved (94% vs 83%). These data show that acclimation to hypoxia has a direct effect on cod myocardial function and/or physiology, and suggest that the cod heart shows some adaptations to prolonged hypoxia.

Section: Resting (Basal) Cardiac Performancesupporting

confidence: 70%

Section: Maximum Cardiac Function: Normoxiamentioning

confidence: 52%

Section: Resting (Basal) Cardiac Performancementioning

confidence: 71%

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In situcardiac function in Atlantic cod (Gadus morhua): effects of acute and chronic hypoxia

Petersen

Gamperl

2010

“…Furthermore, anoxia tolerance in lower vertebrates is usually associated with cold rather than the 22°C used with tilapia. However, a Q 10 value of 2.1 is known for lactate efflux, and thus for glycolytic capacity in rainbow trout heart (Overgaard et al, 2004). Using this Q 10 value, the measured cardiac MGP of the anoxia-tolerant crucian carp at 8°C (79nmol ATPs ).…”

Section: A Comparison Of Maximum Glycolytic Potential Across Speciesmentioning

confidence: 99%

Exceptional cardiac anoxia tolerance in tilapia (Oreochromis hybrid)

Lague¹,

Speers‐Roesch

Richards

et al. 2012

Self Cite

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.

“…Studies to date lend only partial insight into the matter. Isolated heart preparations from brook trout (Salvelinus fontinalis), sea raven (Hemitripertus americanus) and rainbow trout can oxidize glucose to CO 2 (Lanctin et al, 1980;Sephton et al, 1990;Milligan, 1991) and under aerobic conditions there is a low rate of lactate production in fish hearts, typically contributing approximately 5% of the total ATP production (Driedzic et al, 1983;Arthur et al, 1992;West et al, 1993;Overgaard et al, 2007;Lague et al, 2012;Speers-Roesch et al, 2013). But these studies do not reveal what proportion of the aerobic ATP production is supported by extracellular glucose.…”

Section: Introductionmentioning

confidence: 99%

Extracellular glucose supports lactate production but not aerobic metabolism in cardiomyocytes from both normoglycemic Atlantic cod (Gadus morhua) and low glycemic short-horned sculpin (Myoxocephalus scorpius)

Clow

Short

Driedzic

2016

Fish exhibit a wide range of species-specific blood glucose levels. How this relates to glucose utilization is yet to be fully realized. Here, we assessed glucose transport and metabolism in myocytes isolated from Atlantic cod (Gadus morhua) and short-horned sculpin (Myoxocephalus scorpius), species with blood glucose levels of 3.7 and 0.57 mmol l −1 , respectively. Glucose metabolism was assessed by the production of 3 H 2 O from [2-3 H]glucose. Glucose metabolism was 3.5-to 6-fold higher by myocytes from Atlantic cod than by those from short-horned sculpin at the same level of extracellular glucose. In Atlantic cod myocytes, glucose metabolism displayed what appears to be a saturable component with respect to extracellular glucose, and cytochalasin B inhibited glucose metabolism. These features revealed a facilitated glucose diffusion mechanism that accounts for between 30% and 55% of glucose entry at physiological levels of extracellular glucose. Facilitated glucose diffusion appears to be minimal in myocytes for short-horned sculpin. Glucose entry by simple diffusion occurs in both cell types with the same linear relationship between glucose metabolism and extracellular glucose concentration, presumably due to similarities in membrane composition. Oxygen consumption by myocytes incubated in medium containing physiological levels of extracellular glucose (Atlantic cod 5 mmol l −1 , short-horned sculpin 0.5 mmol l −1 ) was similar in the two species and was not decreased by cytochalasin B, suggesting that these cells have the capability of oxidizing alternative on-board metabolic fuels. Cells produced lactate at low rates but glycogen levels did not change during the incubation period. In cells from both species, glucose utilization assessed by both simple chemical analysis of glucose disappearance from the medium and 3 H 2 O production was half the rate of lactate production and as such extracellular glucose was not available for oxidative metabolism. Overall, extracellular glucose makes only a minor contribution to ATP production but a sustained glycolysis may be necessary to support Ca 2+ transport mechanisms at either the sarcoplasmic reticulum or the sarcolemmal membrane.