Abstract
Chronic pressure or volume overload can cause the vertebrate heart to remodel. The hearts of fish remodel in response to seasonal temperature change. Here we focus on the passive properties of the fish heart. Building upon our previous work on thermal-remodeling of the rainbow trout ventricle, we hypothesized that chronic cooling would initiate fibrotic cardiac remodeling, with increased myocardial stiffness, similar to that seen with pathological hypertrophy in mammals. We hypothesized that, in contrast to pathological hypertrophy in mammals, the remodeling response in fish would be plastic and the opposite response would occur following chronic warming. Rainbow trout held at 10°C (control group) were chronically (>8 weeks) exposed to cooling (5°C) or warming (18°C). Chronic cold induced hypertrophy in the highly trabeculated inner layer of the fish heart, with a 41% increase in myocyte bundle cross-sectional area, and an up-regulation of hypertrophic marker genes. Cold acclimation also increased collagen deposition by 1.7-fold and caused an up-regulation of collagen promoting genes. In contrast, chronic warming reduced myocyte bundle cross-sectional area, expression of hypertrophic markers and collagen deposition. Functionally, the cold-induced fibrosis and hypertrophy were associated with increased passive stiffness of the whole ventricle and with increased micromechanical stiffness of tissue sections. The opposite occurred with chronic warming. These findings suggest chronic cooling in the trout heart invokes a hypertrophic phenotype with increased cardiac stiffness and fibrosis that are associated with pathological hypertrophy in the mammalian heart. The loss of collagen and increased compliance following warming is particularly interesting as it suggests fibrosis may oscillate seasonally in the fish heart, revealing a more dynamic nature than the fibrosis associated with dysfunction in mammals.
Highlights
Chronic changes in pressure or volume load can cause the vertebrate heart to change in size, form and function (Clark and Rodnick, 1999; Opie et al, 2006)
There was no difference in total ventricular mass or ventricular mass relative to body mass (RVM) between the three temperature acclimation groups (Table 1)
Cold-induced spongy hypertrophy and warm-induced spongy atrophy were supported by changes in mRNA expression of muscle-specific growth genes (Figure 1F) with ventricular myosin heavy chain (VMHC) 10.3-fold higher, muscle LIM protein (MLP) 6.1fold higher, and small myosin light chain 2 (SMLC2) 7.4-fold higher in cold- compared with warm-acclimated spongy myocardium (P < 0.05, Figure 1F)
Summary
Chronic changes in pressure or volume load can cause the vertebrate heart to change in size, form and function (Clark and Rodnick, 1999; Opie et al, 2006). Hypertrophy of the mammalian left ventricle can improve cardiac performance to meet increased demands such as those occurring with pregnancy or following exercise training (Mone et al, 1996). This “physiological” hypertrophy increases ventricular wall thickness in line with chamber radius causing both stroke volume and systolic pressure to increase, improving overall cardiac output (Dorn, 2007; Bernardo et al, 2010). Pathological remodeling is persistent and is associated with various cardiomyopathies including myocardial infarction, arrhythmia, and sudden death (Bernardo et al, 2010)
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