Exceptional cardiac anoxia tolerance in tilapia (Oreochromis hybrid)

Abstract

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.

Evidence for a role of heme oxygenase-1 in the control of cardiac function in zebrafish (Danio rerio) larvae exposed to hypoxia

“…In sham-treated zebrafish larvae exposed to hypoxia, diastolic volume was decreased without a change in systolic volume, which, when coupled with an increase in f H , resulted in sustained cardiac performance. Sustained cardiac performance during hypoxia also was reported in tilapia (Oreochromis hybrid), which compensated for a decrease in f H induced by severe hypoxia by elevating SV and thus maintained _ Q (Lague et al, 2012). Based on our results, HO-1-deficient larvae were also able to maintain normoxic SV and _ Q under hypoxic conditions.…”

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

“…Maximum adrenergic stimulation (up to 500nmoll -1 ) has no effect on either heart rate or maximum Q, and only a modest (10-15%) positive inotropic effect on power output of the in situ sea bass (Dicentrarchus labrax) heart at 18 and 22°C (Farrell et al, 2007). Finally, Lague et al (Lague et al, 2012) report that AD and noradrenaline concentrations as high as 5ϫ10 -6 moll -1 have no effect on function of the 22°C in situ tilapia (Oreochromis hybrid) heart under conditions of normoxia, hypoxia or acidosis.…”

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)

“…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.…”