Search

Although neural modulation of heart rate is well established among chordate animals, the Pacific hagfish (Eptatretus stoutii) lacks any cardiac innervation, yet it can increase its heart rate from the steady, depressed heart rate seen in prolonged anoxia to almost double its normal normoxic heart rate, an almost fourfold overall change during the 1-h recovery from anoxia. The present study sought mechanistic explanations for these regulatory changes in heart rate. We provide evidence for a bicarbonate-activated, soluble adenylyl cyclase (sAC)-dependent mechanism to control heart rate, a mechanism never previously implicated in chordate cardiac control.

Hypoxia and increased temperature alter venous blood pressures in teleosts through active changes in venous tone. Elasmobranchs possess a capacious venous system but have limited adrenergic vascular innervation and subambient central venous pressure ([P.sub.cv]). In this study, we explored venous hemodynamic responses to acute temperature increase and moderate (6.9 kPa) and severe (2.5 kPa) hypoxia in the dogfish (Squalus acanthias). Normoxic dogfish at 10[degrees]C had a [P.sub.cv] between -0.08 and -0.04 kPa and a mean circulatory filling pressure ([P.sub.mcf]) of ~0.12 kPa. At 16[degrees]C, heart rate ([f.sub.H]), cardiac output (Q), and [P.sub.mcf] increased but [P.sub.cv] and plasma epinephrine and norepinephrine levels were unchanged. In contrast, moderate and severe hypoxia increased [P.sub.cv] and decreased Q and stroke volume ([V.sub.s]). [f.sub.H] decreased in severe hypoxia, whereas [P.sub.mcf] was unaffected despite elevated catecholamine levels. Atropine abolished hypoxic reductions in Q, [V.sub.s], and [f.sub.H], but [P.sub.cv] still increased. In contrast to the response in teleosts, this study on dogfish suggests that venous capacitance changes associated with warming and hypoxia are minimal and likely not mediated by circulating catecholamines. Thus hemodynamic status of the capacious elasmobranch venous circulation is potentially regulated by blood volume shifts from passive flow-mediated events and possibly through myogenic mechanisms. cardiac filling; cardiac performance; elasmobranch; mean circulatory filling pressure

This study was undertaken to provide a comprehensive set of data relevant to disclosing the physiological effects and possible oxygen transport limitations in the Chinook salmon (Oncorhynchus tshawytscha) during an acute temperature change. Fish were instrumented with a blood flow probe around the ventral aorta and catheters in the dorsal aorta and sinus venosus. Water temperature was progressively increased from 13[degrees]C in steps of 4[degrees]C up to 25[degrees]C. Cardiac output increased from 29 to 56 ml x [min.sup.-1] x [kg.sup.-1] between 13 and 25[degrees]C through an increase in heart rate (58 to 105 beats/min). Systemic vascular resistance was reduced, causing a stable dorsal aortic blood pressure, yet central venous blood pressure increased significantly at 25[degrees]C. Oxygen consumption rate increased from 3.4 to 8.7 mg x [min.sup.-1] x [kg.sup.-1] during the temperature increase, although there were signs of anaerobic respiration at 25[degrees]C in the form of increased blood lactate and decreased pH. Arterial oxygen partial pressure was maintained during the heat stress, although venous oxygen partial pressure ([MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII]) and venous oxygen content were significantly reduced. Cardiac arrhythmias were prominent in three of the largest fish (>4 kg) at 25[degrees]C. Given the switch to anaerobic metabolism and the observation of cardiac arrhythmias at 25[degrees]C, we propose that the cascade of venous oxygen depletion results in a threshold value for [MATHEMATICAL EXPRESSION NOT REPRODUCIBLE IN ASCII] of around 1 kPa. At this point, the oxygen supply to systemic and cardiac tissues is compromised, such that the oxygen-deprived and acidotic myocardium becomes arrhythmic, and blood perfusion through the gills and to the tissues becomes compromised. blood pressure; blood respiratory properties; cardiac output; hematocrit; hemoglobin; heart rate; blood plasma; rate of oxygen consumption; oxygen equilibrium curves; Pacific salmon; stroke volume; vascular resistance

Pacific hagfish, Eptatretus stoutii, can recover from 36 h of anoxia at 10°C. Such anoxia tolerance demands the mobilization of anaerobic fuels and the removal of metabolic wastes -- processes that require a functional heart. The purpose of this study was to measure the metabolic response of the excised, cannulated hagfish heart to anoxia using direct calorimetry. These experiments were coupled with measurements of cardiac pH and metabolite concentrations, at multiple time points, to monitor acid-base balance and anaerobic ATP production. We also exposed hagfish to anoxia to compare the in vitro responses of the excised hearts with the in vivo responses. The calorimetry results revealed a significant reduction in the rate of metabolic heat production over the first hour of anoxia exposure, and a recovery over the subsequent 6 h. This response is likely attributable to a rapid anoxia-induced depression of aerobic ATP-production pathways followed by an upregulation of anaerobic ATP-production pathways such that the ATP production rate was restored to that measured in normoxia. Glycogen-depletion measurements suggest that metabolic processes were initially supported by glycolysis but that an alternative fuel source was used to support the sustained rates of ATP production. The maintenance of intracellular pH during anoxia indicates a remarkable ability of the myocytes to buffer/regulate protons and thus protect cardiac function. Altogether, these results illustrate that the low metabolic demand of the hagfish heart allows for near-routine levels of cardiac metabolism to be supported anaerobically. This is probably a significant contributor to the hagfish's exceptional anoxia tolerance. [ABSTRACT FROM AUTHOR]

In the absence of any previous study of the cardiac status of hagfishes during prolonged anoxia and because of their propensity for oxygen-depleted environments, the present study tested the hypothesis that the Pacific hagfish Eptatretus stoutii maintains cardiac performance during prolonged anoxia. Heart rate was halved from the routine value of 10.4±1.3 beats min-1 by the sixth hour of an anoxic period and then remained stable for a further 30h. Cardiac stroke volume increased from routine (1.3±0.1 ml kg-1) to partially compensate the anoxic bradycardia, such that cardiac output decreased by only 33% from the routine value of 12.3±0.9mlmin-1 kg-1. Cardiac power output decreased by only 25% from the routine value of 0.26±0.02mWg-1. During recovery from prolonged anoxia, cardiac output and heart rate increased to peak values within 1.5 h. Thus, the Pacific hagfish should be acknowledged as hypoxic tolerant in terms of its ability to maintain around 70% of their normoxic cardiac performance during prolonged anoxia. This is only the second fish species to be so classified. [ABSTRACT FROM AUTHOR]