Alterations in gill structure in tropical reef fishes as a result of elevated temperatures.

Tropical regions are expected to be some of the most affected by rising sea surface temperatures (SSTs) because seasonal temperature variations are minimal. As temperatures rise, less oxygen dissolves in water, but metabolic requirements of fish and thus, the demand for effective oxygen uptake, increase. Gill remodelling is an acclimation strategy well documented in freshwater cyprinids experiencing large seasonal variations in temperature and oxygen as well as an amphibious killifish upon air exposure. However, no study has investigated whether tropical reef fishes remodel their gills to allow for increased oxygen demands at elevated temperatures. We tested for gill remodelling in five coral reef species (Acanthochromis polyacanthus, Chromis atripectoralis, Pomacentrus moluccensis, Dascyllus melanurus and Cheilodipterus quinquelineatus) from populations in northern Papua New Guinea (2° 35.765' S; 150° 46.193' E). Fishes were acclimated for 12-14 days to 29 and 31°C (representing their seasonal range) and 33 and 34°C to account for end-of-century predicted temperatures. We measured lamellar perimeter, cross-sectional area, base thickness, and length for five filaments on the 2nd gill arches and qualitatively assessed 3rd gill arches via scanning electron microscopy (SEM). All species exhibited significant differences in the quantitative measurements made on the lamellae, but no consistent trends with temperature were observed. SEM only revealed alterations in gill morphology in P. moluccensis. The overall lack of changes in gill morphology with increasing temperature suggests that these near-equatorial reef fishes may fail to maintain adequate O2 uptake under future climate scenarios unless other adaptive mechanisms are employed.

Regulation of the cardiorespiratory system of common carp (Cyprinus carpio) during severe hypoxia at three seasonal acclimation temperatures.

Little is known of the cardiorespiratory control mechanisms utilized by hypoxia-tolerant teleost fish to tolerate prolonged periods (h) of near anoxic exposure. Here, we report on the cardiorespiratory control mechanisms of the common carp Cyprinus carpio L. during normoxia and prolonged, severe hypoxic (<0.3 mg O(2) L(-1)) exposure at acclimation temperatures of 5 degrees C, 10 degrees C, and 15 degrees C. Through serial intra-arterial injections of alpha - and beta -adrenergic, cholinergic, and purinergic antagonists while measuring cardiac output (Q), heart rate (f(H)), ventral aortic blood pressure, and respiration rate, we established that autonomic cardiovascular and respiratory control was preserved during severe hypoxia at all three acclimation temperatures and contributed to downregulation of cardiorespiratory activity. Specifically, inhibitory cholinergic tone mediated up to 76% reductions in f(H) and Q during hypoxia, whereas the accompanying arterial hypotension was attenuated by an upregulation of an alpha -adrenergically mediated peripheral vasoconstriction. Despite the overall cardiac downregulation, a large, stimulatory cardiac beta -adrenergic tone was present during prolonged, severe hypoxia, possibly to protect the heart from attendant acidotic conditions. Purinergic blockade, following alpha -adrenergic and cholinergic antagonists, showed that the hypoxic ventilatory depression, which reversed the 2.3- to 7.7-fold increases in respiration rate that occurred with the onset of hypoxia, was a result of purinergic inhibition at all three acclimation temperatures. In contrast, purinergic inhibition of cardiac activity during hypoxia might be important only at 5 degrees C. Finally, given that cardiac power output was reduced 72%-87% during prolonged, severe hypoxia and that glycolysis yields approximately 94% less ATP per mole glucose than oxidative phosphorylation, it seems unlikely that the common carp sufficiently reduces its cardiac energy demand to a level to preclude activation of a partial Pasteur effect. This means that glycogen stores will be used and waste products will accumulate at faster rates, a finding that may help explain why the common carp cannot tolerate such extended periods of severe hypoxia (weeks to months) at cold acclimation temperatures as the freshwater turtle, which is able to reduce its cardiac energy demand to a level that does not require a Pasteur effect and also blunts autonomic cardiovascular control.

Alpha-adrenergic regulation of systemic peripheral resistance and blood flow distribution in the turtle Trachemys scripta during anoxic submergence at 5 degrees C and 21 degrees C.

Anoxic exposure in the anoxia-tolerant freshwater turtle is attended by substantial decreases in heart rate and blood flows, but systemic blood pressure (P(sys)) only decreases marginally due to an increase in systemic peripheral resistance (R(sys)). Here, we investigate the role of the alpha-adrenergic system in modulating R(sys) during anoxia at 5 degrees C and 21 degrees C in the turtle Trachemys scripta, and also describe how anoxia affects relative systemic blood flow distribution (%.Q(sys)) and absolute tissue blood flows. Turtles were instrumented with an arterial cannula for measurement of P(sys) and ultrasonic flow probes on major systemic blood vessels for determination of systemic cardiac output ((.Qsys)). Alpha-adrenergic tone was assessed from vascular injections of alpha-adrenergic agonists and antagonists (phenylephrine and phentolamine, respectively) during normoxia and following either 6 h (21 degrees C) or 12 days (5 degrees C) of anoxic submergence. Coloured microspheres, injected through a left atrial cannula during normoxia and anoxia, as well as after alpha-adrenergic stimulation and blockade during anoxia at both temperatures, were used to determine relative and absolute tissue blood flows. Anoxia was associated with an increased R(sys) and functional alpha-adrenergic vasoactivity at both acclimation temperatures. However, while anoxia at 21 degrees C was associated with a high systemic alpha-adrenergic tone, the progressive increase of R(sys) at 5 degrees C was not mediated by alpha-adrenergic control. A redistribution of blood flow away from ancillary vascular beds towards more vital circulations occurred with anoxia at both acclimation temperatures. %.Q(sys) and absolute blood flow were reduced to the digestive and urogenital tissues (approximately 2- to 15-fold), while %.Q(sys) and absolute blood flows to the heart and brain were maintained at normoxic levels. The importance of liver and muscle glycogen stores in fueling anaerobic metabolism were indicated by increases in %.Q(sys) to the muscle at 21 degrees C (1.3-fold) and liver at 5 degrees C (1.7-fold). As well, the crucial importance of the turtle shell as a buffer reserve during anoxic submergence was indicated by 40-50% of .Q(sys) being directed towards the shell during anoxia at both 5 degrees C and 21 degrees C. Alpha-adrenergic stimulation and blockade during anoxia caused few changes in %.Q(sys) and absolute tissue blood flow. However, there was evidence of alpha-adrenergic vasoactivity contributing to blood flow regulation to the liver and shell during anoxic submergence at 5 degrees C.

Cardiorespiratory responses of the common carp (Cyprinus carpio) to severe hypoxia at three acclimation temperatures.

In vivo measurements of the cardiovascular responses of anoxia-tolerant teleosts to severe prolonged hypoxia are limited. Here, we report the first direct measurements of cardiac output (Q), heart rate (f(H)) and stroke volume during prolonged severe hypoxia (<0.3 mg O(2) l(-1)) in common carp (Cyprinus carpio L.) that had been acclimated to 6, 10 and 15 degrees C. While routine Q and f(H) values varied with temperature under normoxic conditions (Q(10) values of 1.7 and 2.6, respectively), severe hypoxic exposure significantly depressed f(H) and Q to similar minimum values that were largely independent of acclimation temperature (Q(10) values of 1.2). In contrast, the duration of cardiac depression and the subsequent time period during which carp could tolerate severe hypoxia were inversely related to acclimation temperature (24 h at 6 degrees C, 6 h at 10 degrees C, and 2.5 h at 6 degrees C). Likewise, respiration rate during hypoxia showed a temperature dependence. An unusual finding was that cardiorespiratory status partially recovered during the latter stages of severe hypoxic exposure. We conclude that the cardiorespiratory responses to severe prolonged hypoxia in common carp involved a mixture of temperature-independent, temperature-dependent and time domain phases.