Interleukin 1 Pretreatment Decreases Ischemia/Reperfusion Injury

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 87; no. 13; pp. 5026 - 5030
• Main Authors: Brown, James M., White, Carl W., Terada, Lance S., Grosso, Michael A., Shanley, Paul F., Mulvin, David W., Banerjee, Anirban, Glenn J. R. Whitman, Harken, Alden H., Repine, John E.
• Format: Journal Article
• Language: English
• Published: Washington, DC National Academy of Sciences of the United States of America 01.07.1990; National Acad Sciences
• Subjects: 6-Aminonicotinamide - pharmacology; Amitrole - pharmacology; Animals; Antioxidants; Biological and medical sciences; Catalase - metabolism; Fundamental and applied biological sciences. Psychology; Glucosephosphate Dehydrogenase - metabolism; Glutathione - analogs & derivatives; Glutathione - analysis; Glutathione Disulfide; Glutathione Peroxidase - metabolism; Glutathione Reductase - metabolism; Heart; Heart - drug effects; Hydrogen Peroxide - metabolism; In Vitro Techniques; Interleukin-1 - pharmacology; Ischemia; Leukocytes - cytology; Leukocytes - pathology; Myocardial Reperfusion Injury - prevention & control; Myocardium - cytology; Myocardium - enzymology; Myocardium - pathology; Neutrophils; Perfusion; Pretreatment; Rats; Rats, Inbred Strains; Recombinant Proteins - pharmacology; Reference Values; Superoxide Dismutase - metabolism; Tungsten; Ventricular function; Vertebrates: cardiovascular system; Vinblastine - pharmacology; Xanthine Dehydrogenase - metabolism; Xanthine Oxidase - metabolism; Xanthines; Heart; Vertebrata; Mammalia; Enzymatic activity; Ischemia; Rat; Enzyme; Neutrophile; Interleukin; Rodentia; Antioxidant; Hydrogen peroxides
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.87.13.5026

Hearts isolated from rats treated 36 hr before with interleukin 1 (IL-1) had increased glucose-6-phosphate dehydrogenase (G6PD) activity and decreased hydrogen peroxide levels and injury after global ischemia (I,20 min)/reperfusion (R,40 min) compared with hearts from untreated rats. Hearts isolated from rats treated 6 hr earlier with IL-1 also had increased polymorphonuclear leukocytes (PMN), H2O2levels, and oxidized glutathione (GSSG) contents compared with hearts from untreated rats. Depletion of circulating blood PMN by prior treatment with vinblastine prevented both early (from treatment 6 hr before study) IL-1-induced increases in myocardial PMN accumulation, H2O2levels, and GSSG contents and late (from treatment 36 hr before study) increases in myocardial G6PD activity and protection against I/R. Our results indicate that IL-1 pretreatment causes an early (6 hr after IL-1 treatment) myocardial PMN accumulation and most likely an H2O2-dependent oxidative stress, which contributes to late (36 hr after IL-1 treatment) increases in myocardial G6PD activity and decreases in I/R injury.