溶存窒素過剰に因る魚のガス病について

(1) In order to clarify the relations between 'gas disease' of fish and the degree of supersaturation of dissolved nitrogen in the medium water, samples of five species of fresh-water fish were exposed to flows of water containing relatively constant high concentrations of nitrogen, and the time taken from the initial exposure until visible signs of the disease appeared on the fish body and the survival time were recorded for individual fish. Experiments were performed at about 20 °C.
(2) Above a certain critical nitrogen level, symptoms characteristic of gas disease develop over the surface of the fish body, though being not necessarily followed by fatal lesions. This critical level is termed here the 'detrimental nitrogen limit'. With further increase in nitrogen concentration, a level is reached where the fish can no longer escape death from gas disease. This level is termed the 'lethal nitrogen limit'. These two limits were defined by determining following two nitrogen levels: the level at which just 50% of the fish developed symptoms of gas disease during the experimental period of two weeks, and the level which just failed to cause 50% mortality within the same period of time. Median latent period (the time that elapsed before gas disease was manifested by external symptoms) and median survival time for samples of fish exposed to various levels of nitrogen were also determined.
(3) Each species of fish affected by gas disease exhibited external symptoms more or less peculiar to itself. In the crucian carp (Carassius auratus) and the carp (Cyprinus carpio) the first indication of the disease was the formation of vesicles of gas in their fin membrane or the protrusion of the eyeballs caused by the accumulation of gas in their orbits. In the bitterling (Rhodeus ocellatus) gas blisters were formed on the fins. In the killifish (Oryzias latipes) the first noticeable sign of the disease was the distention of the abdomen owing to the accumulation of gas in the air-bladder, the intestine or the abdominal cavity, which produced considerable buoyancy so as to lift the body up to the surface of the water. In the eel (Anguilla japonica) the first indication of the disease was the development of several small swellings filled with gaseous content on the head.
(4) The immediate cause of death was usually asphyxiation from gas embolism in the circulatory system. But the killifish, especially the fry and young, died very often from the laceration in the abdominal wall, which was caused by an expansive pressure of the gas accumulated in the air-bladder and so forth.
(5) The detrimental nitrogen limit varied to some extent according to species and growth of fish, being estimated to be about 125 96 of air saturation for adult crucian carp and the eel, and about 130% for young crucian carp, young carp, the killifish and the bitterling.
(6) The lethal nitrogen limit differed considerably with species and growth of fish. The values obtained for the fish used were approximately: 120% for adult carp, 125% for adult crucian carp, 130% for eel and young carp, 135% for bitterling and young crucian carp, and a little over 140% for killifish.
(7) From these figures and some other experiments it was learned that smaller fish tended to be more tolerant and resistant to supersaturation of nitrogen than larger ones. It was also suggested that at nitrogen levels below 115% of air saturation almost every fish could survive indefinitely without showing any sign of gas disease.
(8) The ability of the fry of the killifish immediately after hatching to resist supersaturation of nitrogen was very low, but it increased gradually as development proceeded. This change appears to be due to an increasing elasticity and tenacity of tissues of the abdominal walls. The increase in resistance ended when fish attained a body length of about 2cm and was replaced by a trend in the opposite direction, owing to changes in susceptibility to gas embolism.
(9) That large fish are less resistant to gas disease, in other words, they are more susceptible to gas embolism than smaller ones, is surmised to be due to stronger muscular activity in the former than in the latter. Because it is known that bubbles of gas occur in blood vessels as a result of the contraction of muscles between which blood vessels pass. The stronger muscular activity must be accompanied by a more active bubble formation in blood vessels.
(10) It is interesting to note that the 'swellings' on the head of the eel are restricted in their positions to develop. Anatomical studies showed that the eel have just twenty small subcutaneous cavities in its head, with which the lateral canals communicate directly by means of openings on their tuberosities. Under the condition of supersaturation of nitrogen, free gas is accumulated in these subcutaneous cavities and forces up the overlying integument, thus producing 'swellings'. Decompression experiments suggested that bubbles occur in these cavities or in the lateral canals as a result of the movement of jaws and opercula.
(11) Observations on the process of gas-blister formation in the fin of the eel showed that contraction of fin-muscles and tension of connective tissues between or around fin-muscles and of tissues of the fin itself have significant relations to the development of gas bubbles there.