Intestinal mitochondrial dysfunction in surgical stress

Abstract

Background: Surgical stress is associated with altered intestinal function. Our earlier study using a rat model indicated that oxidative stress plays an important role in this process. Since mitochondria are crucial to cellular function and survival and are both a target as well as a source of reactive oxygen species, the present study looks at the changes in enterocyte mitochondria during surgical stress. Methods: Surgical stress was induced by opening the abdominal wall and handling the intestine as done during laparotomy. Mitochondria were prepared from the isolated enterocytes at different time periods after surgical stress. The effect of surgical stress on enterocyte mitochondrial ultrastructure, respiration, anti-oxidant enzyme activity, thiol redox status, calcium flux, permeability, and matrix enzymes was then studied. Results: Surgical stress resulted in alterations in mitochondrial respiration and thiol redox status. It was also associated with altered mitochondrial matrix enzyme activity, decreased superoxide dismutase activity, induction of mitochondrial permeability transition, and swelling, as well as impairment of mitochondrial calcium flux. These alterations were seen at a maximum of 60 min following surgical stress and were reversed by 24 h. Conclusions: Laparotomy and mild intestinal handling itself results in enterocyte mitochondrial damage. Since mitochondria are important cellular organelles, this damage can probably lead to compromised intestinal function.