title: Intestinal, hepatic and renal production of thiobarbituric acid reactive substances and myeloperoxidase activity after temporary aortic occlusion and reperfusion.
abstract: Ischemia induced oxygen free radical damage was formerly attributed only to xanthine oxidase in intestine, liver, kidney and heart. A reevaluation indicated neutrophils as one of the major sources of postischemic oxidative tissue damage, chiefly in the intestine. Our data, obtained from the same occlusion time period for intestine, liver and kidney, showed a certain oxidative damage in intestine and kidney already during ischemia, expressed by an increase of thiobarbituric acid reactive substances (TBARS), whereas the liver sustained damage of this kind only during reperfusion. Oxidative stress was expressed by a comparison of the increase of TBARS, though this test is not a measure of a specific product of lipid peroxidation, but rather comprises several breakdown products of free radical damage. Myeloperoxidase as measure of neutrophil stimulation increased in the intestine and liver. The kidney sustained damage without an increase of myeloperoxidase activity, but showed a similar pattern of increase of TBARS as in the intestine. Our data suggest a major role of neutrophils in intestinal ischemia induced damage, where neutrophils can effect initiation and propagation. In the liver neutrophils may play a minor role concerning propagation, but they may act as an important initiating mechanism. Hepatic tissue shows a high ischemic tolerance, which is demonstrated by a missing increase of TBARS in spite of a certain increase of myeloperoxidase activity during ischemia. This can be interpreted by the high capacity of antioxidative mechanisms of liver tissue and the ability of a higher oxygen extraction ratio under nearly ischemic conditions. In the kidney there appears a smaller contribution of neutrophils. The similar pattern of increase of TBARS in kidney and intestine demonstrates a comparable low ischemic tolerance of these two tissues, whereas different initiating and propagating systems may occur.
authors.affiliation: Physiologisches Institut, Universität Würzburg, FRG.
authors.forename: A J
authors.initials: AJ
authors.lastname: Augustin
authors.forename: J
authors.initials: J
authors.lastname: Lutz
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism*; D001157:Arterial Occlusive Diseases / Q000201:enzymology / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000098:blood supply / Q000201:enzymology; D007511:Ischemia / Q000201:enzymology / Q000378:metabolism; D007668:Kidney / Q000098:blood supply / Q000201:enzymology / Q000378:metabolism*; D015227:Lipid Peroxidation; D008099:Liver / Q000098:blood supply / Q000201:enzymology / Q000378:metabolism*; D008297:Male; D009195:Peroxidase / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D015424:Reperfusion; D013858:Thiobarbiturates / Q000378:metabolism*
chemical_list: D013858:Thiobarbiturates; D009195:Peroxidase; C029684:thiobarbituric acid