Decapod crustacean hearts are suspended by a three-dimensional array of alary ligaments. These ligaments are stretched during systole; diastolic filling via the ostia occurs as the ventricle is stretched by ligamental elastic recoil. There is no direct venous return to the hearts in these animals. In the present study, an isolated heart preparation with intact ligaments, hereafter called in situ, was used to evaluate the effects of artificially induced stretch on heart rate. Strongly beating in situ neurogenic hearts of the crab Carcinus maenas responded to direct perfusion of the ventricle with oxygenated saline and the attendant augmentation of natural stretch with a small increase in heart rate (fh); however, fh was well maintained for up to 15 min after eliminating stretch by cutting the alary ligaments. In contrast to crabs, high rates of artificial perfusion usually depressed fh in crayfish hearts. Crab heart rate falls during hypoxia and this is readily reversed by even low rates of perfusion with oxygenated saline. It is concluded that the gradual decline in fh of totally isolated in vitro hearts arises from the deepening intraventricular hypoxia experienced by the cardiac ganglion.

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