Effect of high sustained +Gz stress on myocardial mitochondrial ultrastructure, respiratory function, and antioxidant capacity in rats.

Exposure to high sustained positive acceleration (+Gz) is known to have a pathophysiological effect on the heart of the rat. As critical regulators of cardiac myocyte survival and death, mitochondria may be crucially involved in +Gz-induced pathogenesis. It was, therefore, of interest to investigate myocardial mitochondrial ultrastructure, respiratory function, and antioxidant capacity in rats after exposure to +10 Gz for 5 min. The results showed that high +Gz stress could damage mitochondrial ultrastructure; this was apparent from swollen, degenerated, and reduced mitochondria, and mitochondrial cristae broken or disappeared. This resulted in significant changes of quantitative indicators of mitochondria morphometry, for example increased surface density, volume density, average volume, and average surface area, and reduced numerical density. The studies also revealed that exposure to +Gz stress induced dysfunction of the mitochondrial respiratory chain, reduced the activity of antioxidant enzymes (catalase, superoxide dismutase, and glutathione peroxidase), and increased malondialdehyde content. We thus conclude that high +Gz stress not only damaged mitochondrial ultrastructure but also impaired respiratory function and antioxidant capacity.