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Work in the last decade has shown that crustacean open circulatory systems are highly efficient and controlled in a complex manner. Control occurs at several levels. Myocardial contraction is initiated in the cardiac ganglion but constantly modulated by the central nervous system, both directly via the cardioregulatory nerves and indirectly via the neurohormonal system. Heart rate and stroke volume can be controlled independently and measurements of both are needed to assess cardiac output accurately. Haemolymph outflow from many arthropod hearts is via a complex multiarterial distribution system, and the regional distribution of cardiac output is tightly controlled via cardioarterial valves at the base of each artery. These valves contain innervated muscle, and differential contraction serves to regulate the efflux of oxygenated haemolymph into a particular system. The major influence on both the evolution and control of arthropod open blood vascular systems is efficiency of oxygen uptake and delivery. This influence is illustrated by reference to a variety of crustacean and other arthropod types.

Peptide neurohormones exist as functionally similar analogues in a wide variety of invertebrate and vertebrate phyla, and many have been implicated as cardiovascular regulators. In decapod crustaceans, these include the pentapeptide proctolin, crustacean cardioactive peptide (CCAP) and the FMRF amide-related peptides F1 and F2, all of which are found in the pericardial organs located immediately upstream of the heart. Cardioexcitatory activity has been demonstrated by these four peptides in both isolated and semi-isolated arthropod hearts; CCAP, however, has minimal effects on the heart of Cancer magister. In the present study, we determined the effects of proctolin, F1 and F2 on the heart of the crab C. magister in both in vitro (semi-isolated heart) and in vivo (whole animal) preparations. In semi-isolated hearts, infusion of each peptide caused cardioexcitation, increasing the rate and stroke volume of the heart. In whole crabs, the peptides were cardioinhibitory; the strongest effects were observed with F1 and F2, which dramatically decreased heart rate, cardiac stroke volume and cardiac output. These results cast doubt on current perceptions of the functional role of cardioactive peptides in the regulation of invertebrate cardiovascular performance in vivo.

Unrestrained, quiescent starry flounder maintained approximately normal levels of O2 uptake in the face of severe experimental anaemia. At haematocrits above about 5%, the only major compensation was a reduction in venous O2 tension which lowered venous saturation and thereby kept a constant difference between arterial and venous O2 contents. Below a haematocrit of about 5%, this difference decreased, and many additional compensations were invoked, including increases in ventilation, expired O2 tension, arterial O2 tension, and cardiac output, and decreases in systemic vascular resistance and blood pH. All changes could be reversed by restoration of haematocrit. Exercise performance and post-exercise changes in blood pH and lactate differed only slightly between anaemic and normal flounder. In wild flounder, anaemia commonly occurs and apparently only causes death at the haematocrit value (about 5%) below which most major compensations are implemented. The respiratory strategy of the flounder during anaemia is compared with that of the rainbow trout.

A wide range of respiratory, ventilatory, and cardiovascular parameters have been recorded under completely resting conditions in the starry flounder (Platichthys stellatus), a generally inactive benthic teleost. The results differ in a number of important respects from those of a previous study on the same species. The present data have also been compared with those reported for the active pelagic rainbow trout (Salmo gairdneri) and for other teleost species. Of particular note in the flounder, relative to the trout, are low arterial and venous PO2's, a low arterial-venous O2 content difference, a low transfer factor and high diffusion gradient for O2 across the gills, a high in vivo blood O2 affinity, a high cardiac output and stroke volume accompanied by a low peripheral vascular resistance, a low ventilation volume, a low ventilation-perfusion ratio, and a low capacity-rate ratio for O2 exchange at the gills. Parameters of CO2 transport and acid-base regulation appear conventional, though blood CO2 contents and lactate concentrations are low. The respiratory strategies of inactive versus active, and benthic versus pelagic teleosts are discussed.

Exhausting activity results in a marked and immediate drop in blood pH which gradually returns to normal over the following 6h. The acidosis is caused largely by elevated Pco2 levels, which vary inversely with pH. Blood lactate concentration increases slowly, reaching a maximum at 2--4h post-exercise, and contributes significantly to the acidosis only late in the recovery period. The slow time course of lactic acid release into the blood permits temporal separation of the peak metabolic acidosis from the peak respiratory acidosis. Evidence is presented that a metabolic acid other than lactic also makes a modest contribution to the pH depression during the recovery period.