Copper and haemocyanin dynamics in aquatic invertebrates

Mechanisms of copper accumulation and detoxification, and of haemocyanin biosynthesis and catabolism, in aquatic arthropods and molluscs are reviewed. Crustacean haemocyanin transports copper in the blood by sequestering additional copper outside the oxygen-binding centre. Large changes in haemocyanin concentration in crustacean blood during moulting and hyposaline exposure generally reflect extracellular volume adjustments rather than biosynthesis and catabolism. Haemocyanin synthesis in decapod crustaceans is stimulated by hypoxia and, in an amphipod, by parasitization. Starvation causes breakdown of haemocyanin. Haemocyanin synthesis occurs principally in the midgut gland of crustaceans and in fixed blood cells (cyanocytes) that are located in certain tissues. It is hypothesized that cyanocytes provide a local oxygen reserve during circulatory arrest. Haemocyanin synthesis occurs primarily in the branchial glands of dibranchiate cephalopods but in the midgut gland of tetrabranchiates. Connective tissue pore cells are proposed as the site of haemocyanin synthesis in gastropods, although similar cells in cephalopod branchial hearts probably catabolize haemocyanin. Crustacean midgut glands contain copper-metallothioneins and glutathione, which donate Cu(I) to apohaemocyanin and function in detoxification and mineralization of excess copper. The physiological significance of high concentrations of quasi-crystalline haemocyanin within vascular spaces of the prosobranch left kidney, opisthobranch blood gland and cephalopod branchial heart appendage is discussed.

Cardiac function and circulation in hagfishes

The hagfish circulation contains a high volume of blood (180 mL∙kg−1) and is remarkable for the number of accessory pumps. Cardiac output from the branchial heart of hagfishes is comparable to that of elasmobranch and most teleost fishes, but blood pressures are considerably lower than in any other vertebrate group. Cardiac output is extremely sensitive to both venous return and ventral aortic pressure (afterload). Owing to the low arterial blood pressures, myocardial power output is lower than for any other vertebrate heart. The concomitant low energy requirement of the myocardium allows ATP generated anaerobically through glycolysis to maintain cardiac output during severe hypoxia. In vivo and in vitro administration of adrenergic agonists and antagonists increase and decrease cardiac performance, respectively. This suggests that the catecholamines that are stored beneath the endothelium of the branchial and portal hearts are involved in the tonic control of cardiac function.