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Anoxic survival and cardiovascular responses of the pacific hagfish, Eptatretus stoutii Cox, Georgina Kimberly

Abstract

To determine if anoxic survival in the Pacific hagfish (Eptatretus stoutii L) is aided by the suppression of metabolic rate, excess post-anoxic oxygen consumption (EPAOC) and key metabolites in the glycolytic pathway were analyzed following anoxic exposures of different durations. As the cardiovascular system reflects the needs of the tissue and thus whole animal metabolic rate, cardiac performance during prolonged anoxia was also examined to gain insight into the anoxic cardiac ATP turnover rate. Hagfish survived 36-h exposure of complete anoxia at 10°C but showed 50% mortality if exposed to anoxia for 48 h. In order to determine if there had been metabolic rate suppression, changes in tissue metabolites were measured during 36 h anoxia exposure and EPAOC was monitored using respirometry. Analysis of EPAOC measurements suggest that hagfish use metabolic rate suppression to enhance anoxia survival during bouts of anoxia greater than 24 h and that metabolic rate was halved during the final third of a 36-h anoxic period. However, analysis of tissue metabolites in the liver, heart, tongue and skeletal muscle showed that glycogen levels were rapidly depleted over the first 6 h, but then stabilized for the duration of the anoxic exposure. Taken together, the results of the respirometry study and metabolic analysis suggest that anoxia survival in E. stoutii is enhanced by metabolic suppression, but that this suppression may occur earlier in the anoxic period than revealed by EPAOC measurements alone. To gain a better understanding of the use of metabolic rate suppression as a means for surviving anoxic exposures, cardiovascular function was examined during a 36-h anoxic exposure. Cardiac output and ventral aortic blood pressure were measured for 36 h of anoxia and through full recovery. Anoxic bradycardia that halved heart rate within 3 h, which then remained stable at 5 bpm for 33 h of anoxia. Cardiac output, however, was reduced by only ~33%, suggesting metabolite, hormone and waste transport remain important during anoxia. Furthermore, cardiac power output remained unchanged during anoxia. Thus, cardiac metabolic rate is not suppressed and its routine cardiac ATP demand is met through glycolysis and circulating blood glucose.

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