The swim bladder is a hydrostatic organ in many teleost fish. It is essentially a gas-filled tubular organ which allows fish to maintain a vertical position in the water column without expanding much energy. In general, fish that dwell in the bottom of their habitat lack swim bladders, as do fish who spend their lives swimming continuously in the open ocean. Swim bladders can also have secondary functions such as sound detection and production. The swim bladder can be clinically important in fish medicine, as it is susceptible to infections and anatomic malformations.

Anatomy and Function

Gases in the swim bladder follow Boyle’s law, namely as pressure increases, the volume of gas decreases. However, in order to maintain neutral buoyancy, fish must maintain the volume of gas in the swim bladder. For small, transient changes in pressure, such as encountered in a quick dive or trip to the surface, the volume of gas in the swim bladder will change according to Boyle’s law. However, when a fish experiences more persistent changes in hydrostatic pressure, the fish will actively add or remove gas from the swim bladder to maintain a constant volume. For example, a fish that moves to deeper waters for several hours will add gas to the swim bladder to compensate for the decrease in volume due to an increase in pressure. Conversely, a fish that moves to shallow waters will remove gas from the swim bladder.

The swim bladder wall is composed of collagen fibers on the outside and a vascularized middle layer enriched with smooth muscle. The inner epithelium of the swim bladder is mostly composed of metabolically active cuboidal cells, but the areas involved in reabsorbing gas from the swim bladder have squamous epithelium. The specialized secretory epithelium of the swim bladder is often called the “gas gland.” The swim bladder develops as a diverticulum from the foregut. In physostomes, the connection of the swim bladder to the gut is maintained by a connecting tube called the pneumatic duct. The pneumatic duct is guarded at its esophageal entrance by a sphincter-like arrangement of striated muscle. Adult physoclists, however, have no communication between the swim bladder and esophagus.

Blood flow to the swim bladder is intimately related to its function, as gas from blood is used to fill the swim bladder lumen. In simplified terms, the rete mirable is responsible for gas secretion into the swim bladder and the resorbent capillary network is responsible for removing gas from the swim bladder. In physostomes, the pneumatic duct artery branches off the coelic artery and supplies both the rete and the resorbent capillary network. The physoclist rete is also supplied by a branch off the coelic artery, the gas gland artery, but in contrast to physostomes, the resorbent capillary network is supplied by branches directly off the dorsal aorta. In both groups, venous drainage from the swim bladder has two routes: veins from the rete mirable join the hepatic portal vein while veins from the resorbent capillary network reach the sinus venosus without entering the hepatic portal circulation. For physoclists, blood gases are the only means of filling the swim bladder. Because of the pneumatic duct, physostomes are also able to regulate swim bladder content by ingesting or expelling air through the esophagus. The degree to which physostomes use atmospheric air to fill the swim bladder varies with species, age, and water conditions.

The ability of fish to secrete blood gases into the swim bladder is due to the concentrating effects of the rete mirable. The anatomy of the rete clearly demonstrates its purpose: diffusion between arterial and venous blood. The rete is a bundle of capillaries where arterioles and venuoles are in close diffusion contact. This contact is maximized by a hexagonal or checkerboard pattern, and the distance between arterial and venous blood streams is about the same as the distance between air and blood in the human lung. Blood entering the rete has the same pH and partial pressure of oxygen (P02) as arterial blood elsewhere in the fish’s body. Venous blood in the rete is acidic and has high PO2. As the arterial blood encounters the venous blood in the rete, oxygen diffuses across its pressure gradient into the arterial blood causing the PO2 in the arterial blood to increase. As blood circulates through the swim bladder, the PO2 is further increased by lactic acid secretion from swim bladder epithelium (“gas gland”) into the blood which acidifies the blood and causes gas to be less soluble. As PO2 increases in the blood circulating through the swim bladder, oxygen is secreted into the swim bladder lumen.

Gas can be removed from the swim bladder by reabsorption into the blood. In reabosrptive areas, the swim bladder epithelium becomes squamous and gas can diffuse according to partial pressure differences. Since venous circulation to the resorbent capillary network is separate from that to the rete, the PO2 of these capillaries will be lower than that found in the swim bladder. Gas is not being constantly reabsorbed, however, because this process can be regulated by varying the amount of blood flow through the resorbent capillary network. Some physoclists have a specialized pocket of the swim bladder devoted to reabsorption called the oval. The oval has a smooth muscle sphincter that can regulate gas entry. So, for example, in an ascending fish, the oval will be opened to allow gas entry. This gas will then contact the resobent capillary network, and diffuse into the blood. Some fish that do not have a discrete oval have a diaphragm with a central opening that separates the resorbent area from the secretory area.

Filling and emptying of the swim bladder are under autonomic control. The inflatory reflex, which results in air being deposited into the swim bladder seems to be induced by situations that increase the specific gravity of the fish or decrease the stretch in the swim bladder wall. Conversely, the “deflatory reflex,” which results in removal of air from the swim bladder, is induced by increase stretch in the swim bladder wall. The secretory epithelium of the swim bladder is modulated by cholinergic vagal fibers, while blood flow through the rete mirable is modulated by sympathetic terminals containing norepinepherine. Sympathetic innervation also modulates the resorbent areas of the swim bladder wall by affecting the contractile state of smooth muscle.

Clinical Importance

Disease of the swim bladder can have economic importance to aquaculture, and can be a problem in ornamental fish. Swim bladder infections due to nematodes, coccidia, and fungi have been documented. Developmental failure of the swim bladder to inflate is common in many cultured fish species. Buoyancy problems in fish have been attributed to issues with swim bladder anatomy, either directly due to the swim bladder or due to other organs indirectly affecting swim bladder function.

A major problem of eel fisheries is the nematode Anguillicola crassus. This parasite is native to Southeast Asia, but has been introduced into Europe and North America. The adult nematodes attach to the swim bladder wall and feed on blood. They lay eggs in the swim bladder lumen, which are then passed through the digestive tract. Being a physostome, the eggs can exit the swim bladder through the pneumatic duct. Infected eels will develop hemorrhagic lesions, fibrosis, and eventually collapse of the swim bladder. A. crassus appears to be more virulent in eels that are not from its native range.

The initial inflation of the swim bladder is a critical event in larval fish development. Some physoclists are considered “transient physostomes,” because during larval development the pneumatic duct exists for swim bladder inflation and then regresses. Swim bladder non inflation (SBN) has become a major obstacle for aquaculture of transient physostomes, and has been seen in “pure physoclists” as well. SBN has been linked to decreased growth rates, increased incidence of spinal deformity, increased susceptibility to stress, and increased mortality rates. The causes of SBN are an active area of research, with environmental contaminants and genetics being studied in a number of species.

Disruption of neutral buoyancy is a common occurrence in fancy goldfish. The Japan Aquaculture Society has described “tenpuku” (capsized) disease in goldfish, more commonly known in the United States as “flip over disease.” This disease is characterized by over inflation of the swim bladder causing the fish to float at the surface upside down. Not only is it uncomfortable for the fish and upsetting to the owner, but this disorder will cause ulcerations if the skin of the fish is exposed to air as a result of such extreme positive buoyancy. There may be multiple causes of tenpuku disease in goldfish including dietary issues, viral or bacterial infections of the swim bladder, swim bladder torsion, neoplasia, anatomic abnormalities, or mechanical obstruction of the pneumatic duct. In some cases, simple treatments such as feeding high fiber foods are effective. More invasive treatments include pneumocystocentesis as needed, surgical implantation of quartz crystal to increase the fish’s specific gravity, or removal of all or part of the caudal lobe of the swim bladder.

Many aspects of swim bladder anatomy have yet to be elucidated for many economically important fish species. Most research on the details of swim bladder anatomy is restricted to a handful of species, yet it is clear that there is a great diversity in swim bladder functional morphology amongst the teleost. Future research into the details of swim bladder innervation and development in a variety of species will further illuminate this amazing structure, and hopefully open more avenues to veterinarians for effective prevention and treatment of swim bladder diseases.

References

Bennett, R. O., Kraeuter, J. N., Woods III, L. C., Lipsky, M. M., & May, E. B. (1987) Histological evaluation of swim bladder non-inflation in striped bass larvae Morone saxatilis. Diseases of Aquatic Organisms, 3, 91-95.

Bowater, R. O., Thomas, A., Shivas, R. G., & Humphrey, J. D. (2003) Deuteromycotic fungi infecting barramundi cod, Cromileptes altivelis (Valenciennes), from Australia. Journal of Fish Diseases, 26, 681-686.

Britt, T., Weisse, C., Weber, E. S., Matzkin, Z., & Klide, A. (2002) Use of pneuomocystoplasty for overinflation of the swim bladder in a goldfish. Journal of the American Veterinary Medical Association, 221(5), 690-693.

Fänge, R. (1983) Gas Exchange in Fish Swim Bladder. Reviews in Physiology, Biochemistry, and Pharmacology, 97, 111-158.

Kardong, K.V., (2002) Vertebrates: Comparative Anatomy, Function, and Evolution (3rd ed). New York: McGraw Hill.

Lewbart, G. A., (2000) Green Peas for Buoyancy Disorders. Exotic DVM, 2, 7.

Matysczak, J. (2006) Gas Bladder 101. Florida Aqua New, 2(2), 2-5.

Perlberg, S. T., Diamant, A., Ofir, R. & Zilberg, D. (2008) Characterization of swim bladder non-inflation (SBN) in angelfish, Pterophyllum scalare (Schultz), and the effect of exposure to methylene blue. Journal of Fish Diseases, 31, 215-228.

Steen, J. B. (1970) The Swim Bladder As a Hydrostatic Organ. In W. S. Hoar & D. J. Randall (Eds.), Fish Physiology (Vol. 4, pp 413 - 443). New York: Acedemic Press.

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