Temporal changes after death in primate diaphragm muscle oxidative enzyme activity.

Abstract

We have previously reported that muscle fibers in fresh samples of the diaphragm muscle of prenatal baboons have moderate to high oxidative capacity and are resistant to fatigue in vitro. These conclusions are in conflict with those of others on diaphragmatic muscle fibers studied in autopsy specimens from human infants. Reasons for these divergent interpretations could include species difference and the use of autopsy specimens rather than fresh tissue samples. We have, therefore, tested whether characteristics of human infant diaphragm muscle fibers differ from those of premature baboons, and whether the use of autopsy specimens alters interpretations of histochemical results. Samples obtained from premature, newborn, or adult baboons were quick-frozen immediately after death or after storage for as long as 24 h. Samples were obtained at autopsy from human infants at 4 to 24 h after death. Histochemical assay for NADH-TR activity was performed on cross sections. Samples from baboons at any age showed deterioration with storage, but the muscles from premature and newborn animals were considerably more susceptible to damage than those of adults. Fibers in human infant diaphragm obtained within 10 h of death looked remarkably similar to those of the infant baboons. However, samples obtained at later times after death showed deterioration and loss of oxidative enzyme activity. We conclude that diaphragmatic muscle fibers of humans and nonhuman primates are similar in enzymatic profile, but that elapsed time after death can reduce the intensity of mitochondrial enzyme assays. The decrement in tissue preservation with elapsed time after death is less pronounced in more mature muscles.