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. Author manuscript; available in PMC: 2015 Apr 20.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2013 Jun 20;33(8):1911–1919. doi: 10.1161/ATVBAHA.113.301591

Figure 2.

Figure 2

Mitochondrial oxidative stress and dysfunction induce mitochondrial aggregation and dyad swelling in the myocardium of lean rats in response to repetitive ischemia. Representative electron micrographs from 10-day sham (A, normal zone [NZ]; D, collateral-dependent zone [CZ]); 10-day RI (B, NZ; E, CZ); and 10-day repetitive ischemia (RI)/rotenone (Rot; C, NZ; F, CZ) rats, respectively (n=3 rats per group). Sham-operated rats showed well-preserved intracellular architectures (A and D). Rot induced mitochondrial aggregation (open arrow), indicating mitochondrial network fusion (C and F). This fusion process might be a mechanism for mitochondria to complement impair in function/bioenergetics for survival. It is also important to note that severe dyad swelling (solid arrow) was observed in Rot-treated rats, suggesting alteration in Ca2+ homeostasis in the myocardium (magnification, ×3000; insets, ×10 000). c indicates capillaries.