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Cardiac remodeling in diploid and triploid rainbow trout (Oncorhynchus mykiss Walbaum) Simonot, Danielle Laurette


The extent, time course and qualitative aspects of cardiac remodeling were studied in rainbow trout (Oncorhynchus my kiss Walbaum) using chemically-induced anemia as the induction method. Injection of phenylhydrazine hydrochloride (PHZ) was used to induce a transient hemolytic anemia which increased routine cardiac output (Q) by 20% when the hematocrit (Hct) was reduced from 23% to 10%. It was therefore hypothesized that prior to cardiac remodeling, rainbow trout may rely on venous oxygen stores rather than compensate with energetically-costly increases of cardiac output. Indeed, after Hct was held at an average Hct of 17% for up to 8 weeks, relative ventricular mass (VM) in diploid anemic rainbow trout increased significantly within two weeks and by 84% after eight weeks. Cardiac remodeling was discovered to be influenced by water temperature. While there was a disproportionate increase in % compact myocardium at 6°C (from 30% to 37%, P<0.05), a proportionate increase resulted at 17°C. Furthermore, radioisotope tracer analysis of coronary vascular volume supports coronary angiogenesis of the compact myocardium during cardiac remodeling, as a 37% increase in rVM doubled coronary vascular volume. The potential benefits of cardiac remodeling were tested in vivo by measuring maximum cardiorespiratory and swimming performance in post-anemic rainbow trout that had recovered their Hct, but retained cardiac hypertrophy. As expected, a 27% higher rVM significantly increased maximum Q and stroke volume by 60%, but without affecting swimming performance, maximal oxygen consumption, heart rate or venous oxygen tension, possibly because the hemoglobin concentration had been fully restored in PHZ-treated fish, despite an equivalent Hct. Triploid rainbow trout, which have enlarged cardiomyocytes, responded similarly to PHZ-treatment as diploids cohorts in terms of the rVM and hematological responses to PHZ, but displayed significant effects of handling stress. Their disproportionate increase in spongy myocardium and lack of an angiogenic response may have restricted oxygen diffusion to the myocardium, helping to explain the significant respiratory distress and mortality in response to handling and PHZ treatment at warm temperatures. Thus, anemia-induced cardiac remodeling in rainbow trout is rapid, substantial and plastic, where increased compact myocardium benefits blood supply to the ventricle via the coronary artery, resulting in improved blood pumping capacity of the heart.

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