title: Adenine nucleotides of ischemic intestine do not reflect injury.
abstract: Warm ischemia of the intestine is a medical emergency which results from mesenteric vascular occlusion. In addition, intestinal transplantation techniques will also inevitably result in intestinal ischemia. The recovery of organ function following ischemia depends on the extent of irreversible damage produced by the ischemia and the extent of reflow upon reperfusion. In some organs energy homeostasis has been found to correlate with organ recovery and graft survival following ischemia-reperfusion. Investigating the usefulness of the determination of adenine and pyridine nucleotides as indicators of the extent of ischemic injury in intestinal segments, we found that after an initial 40% decrease in ATP following 30 min of ischemia there was no further decrease despite increasing the ischemia period to 120 min. Similarly, the decrease in NAD+ and NADP which occurred after 30 min of ischemia did not decrease further after 60, 90, or 120 min of ischemia. Xanthine was the only biochemical where an increase appeared to correlate with ischemia duration while energy charge was of no value in indicating injury extent. Additionally, after reperfusion there was at best a poor correlation between recovery of ATP content and the duration of ischemia. Microcirculation reflow after reperfusion indicated ischemia time-related endothelial cell injury. Thus, the measurement of high-energy phosphates in intestinal segments is not of value as an indicator of the extent of intestinal ischemic injury.
authors.affiliation: Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina 27710.
authors.forename: A T
authors.initials: AT
authors.lastname: Canada
authors.forename: L R
authors.initials: LR
authors.lastname: Coleman
authors.forename: M A
authors.initials: MA
authors.lastname: Fabian
authors.forename: R R
authors.initials: RR
authors.lastname: Bollinger
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism*; D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D006358:Hot Temperature; D019271:Hypoxanthine; D007042:Hypoxanthines / Q000378:metabolism; D007410:Intestinal Diseases / Q000209:etiology / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000150:complications / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D009243:NAD / Q000378:metabolism; D009249:NADP / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015424:Reperfusion; D013997:Time Factors; D019820:Xanthine; D014970:Xanthines / Q000378:metabolism
chemical_list: D000227:Adenine Nucleotides; D007042:Hypoxanthines; D014970:Xanthines; D009243:NAD; D019820:Xanthine; D019271:Hypoxanthine; D000249:Adenosine Monophosphate; D009249:NADP; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate