Previous studies have shown that bycaught loggerhead turtles (Caretta caretta) may experience decompression sickness (DCS)1 that results in severe trauma and/or death5. The current work investigated the pulmonary vascular system in loggerhead turtles to determine the anatomical and functional characteristics of the arteries, the pulmonary artery sphincter, and the lung parenchyma. Pulmonary arteries and lungs were excised in 5 turtles that were euthanized due to severe trauma associated with fisheries interactions. Histologically, the tunica intima of the sphincter had a rougher surface and thicker wall as compared with the pulmonary artery. The tunica media of the sphincter was made up of a thick layer of smooth muscle cells and elastic tissue. The presence of muscarinic and adrenergic receptors was confirmed using immunohistochemistry and western blots. The pulmonary artery and sphincter were cut in cylindrical segments of 3- to 5-mm thickness. Each ring was mounted on stirrups made out of stainless steel wire and submerged in a temperature-controlled organ bath. One stirrup was fixed at the bottom and the other attached to a force transducer, which allowed the force of contraction to be measured. The vessel ring was exposed to acetylcholine, serotonin, or epinephrine to determine the neural responses. The sphincter contracted forcefully in response to acetylcholine (parasympathetic response) and also to serotonin, but epinephrine (sympathetic tone) caused relaxation. Epinephrine also induced relaxation even under the effect of acetylcholine. The remainder of the pulmonary artery responded similarly to the sphincter area, but less forcefully during contraction and relaxed less when exposed to epinephrine. We also tried experiments on systemic arteries from C. caretta and on pulmonary artery from pond sliders (Trachemys scripta) and, as opposed to the response we found in the sphincter, all responses were contractive. In addition, the pulmonary parenchyma contains an unusual amount of smooth muscle that contracts in response to acetylcholine but also in response to epinephrine. We believe that these mechanisms provide a possible explanation to the observed DCS in turtles.
Our hypothesis is that during normal dives,2,3,6 the turtles contract the lung and sphincter (under parasympathetic response), which minimizes uptake of N2 and risk of DCS. Parasympathetic response also decreases heart rate and perfusion. During a stressful event, like being caught in a trawler or a net,4,5 the sympathetic response opens the sphincter, resulting in increased lung perfusion, which may increase the risk of DCS. The present study contributes to the functional and anatomic characterisation of this structure described in apneic diving species, and gives new information about the pathophysiology of DCS in sea turtles. This knowledge may help mitigate DCS risk in turtles.
This work was carried out under the auspices of a collaborative agreement on physiology studies in sea mammals between The Oceanogràfic Park of the Ciudad de las Artes y las Ciencias of Valencia and the Research Foundation of the General Hospital from Valencia, Spain. We thank all the team from the Research Foundation at the General Hospital for technical assistance. Funding for this project was provided by the Office of Naval Research (ONR YIP Award # N000141410563).
* Presenting author
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