Intestinal mitochondrial dysfunction in surgical stress

Citation
A. Ramachandran et al., Intestinal mitochondrial dysfunction in surgical stress, J SURG RES, 99(1), 2001, pp. 120-128
Citations number
48
Categorie Soggetti
Surgery,"Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF SURGICAL RESEARCH
ISSN journal
00224804 → ACNP
Volume
99
Issue
1
Year of publication
2001
Pages
120 - 128
Database
ISI
SICI code
0022-4804(200107)99:1<120:IMDISS>2.0.ZU;2-X
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 cellul ar function and survival and are both a target as well as a source of react ive oxygen species, the present study looks at the changes in enterocyte mi tochondria during surgical stress. Methods. Surgical stress was induced by opening the abdominal mall and hand ling the intestine as done during laparotomy. Mitochondria were prepared fr om 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 flu x, permeability, and matrix enzymes was then studied. Results. Surgical stress resulted in alterations in mitochondrial respirati on and thiol redox status. It was also associated with altered mitochondria l matrix enzyme activity, decreased superoxide dismutase activity, inductio n of mitochondrial permeability transition, and swelling, as well as impair ment of mitochondrial calcium flux. These alterations were seen at a maximu m of 60 min following surgical stress and were reversed by 24 h. Conclusions. Laparotomy and mild intestinal handling itself results in ente rocyte mitochondrial damage. Since mitochondria are important cellular orga nelles, this damage can probably lead to compromised intestinal function. ( C) 2001 Academic Press.