title: Thermal preconditioning protects the human internal mammary artery from hypoxia/re-oxygenation-induced damage.
abstract: 1. Preconditioning has been demonstrated to ameliorate ischaemia/reperfusion injury in several cells and tissues. Therefore, in the present study we investigated whether preconditioning of human bypass grafts, internal mammary artery (IMA) and saphenous vein (SV) induces heat shock protein (Hsp) expression and reduces apoptosis in response to subsequent hypoxia/re-oxygenation damage in both vessels. 2. Internal mammary artery and SV rings, obtained from 30 patients (median age 66.5 years) undergoing coronary artery bypass grafting, were either incubated for 30 min at 42 degrees C (preconditioned) or kept in a standard incubator at 37 degrees C (not preconditioned). Six hours later, graft segments were exposed to 90 min hypoxia followed by a 30 min re-oxygenation period. Western blot, real-time quantative polymerase chain reaction analysis and apoptosis detection by the Terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick end-labelling method were performed. 3. Heat-preconditioned IMA showed significantly increased protein expression of Hsp72 after hypoxia/re-oxygenation treatment compared with controls (median 9.1 vs 5.0 microg/mg total protein; P = 0.048). Expression of Hsp73 was weak and Hsp60 was not detectable in the IMA. 4. In the SV, neither protein nor mRNA expression of Hsp were significantly different between preconditioned and not preconditioned veins. 5. There were significantly fewer apoptotic cells in the intima of the preconditioned compared with not preconditioned IMA (P = 0.041) after hypoxia/re-oxygenation injury, whereas in the SV apoptosis was not significantly prevented by preconditioning. 6. Mild heat preconditioning before hypoxia/re-oxygenation injury is a stimulus for Hsp72 protein expression and a reduction in apoptosis in the human IMA.
authors.affiliation: Division of Clinical Biochemistry, Biocenter, Innsbruck Medical University, Innsbruck, Austria. Angelika.Hammerer-Lercher@tilak.at
authors.forename: Angelika
authors.initials: A
authors.lastname: Hammerer-Lercher
authors.forename: Christa
authors.initials: C
authors.lastname: Haeusler
authors.forename: Martina
authors.initials: M
authors.lastname: Prelog
authors.forename: Johannes
authors.initials: J
authors.lastname: Bonatti
authors.forename: Daniel
authors.initials: D
authors.lastname: Hoefer
authors.forename: Elfriede
authors.initials: E
authors.lastname: Ruttmann
authors.forename: Guenther
authors.initials: G
authors.lastname: Laufer
authors.forename: Ernst R
authors.initials: ER
authors.lastname: Werner
authors.forename: Stephan
authors.initials: S
authors.lastname: Dirnhofer
authors.forename: Bernd
authors.initials: B
authors.lastname: Puschendorf
authors.forename: Johannes
authors.initials: J
authors.lastname: Mair
mesh_terms: D000368:Aged; D017209:Apoptosis; D015687:Cell Hypoxia; D001026:Coronary Artery Bypass / Q000379:methods; D005786:Gene Expression Regulation; D050884:HSP72 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism*; D006358:Hot Temperature; D006801:Humans; D066298:In Vitro Techniques; D019194:Ischemic Preconditioning / Q000379:methods; D008323:Mammary Arteries / Q000378:metabolism* / Q000473:pathology; D008875:Middle Aged; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D012501:Saphenous Vein / Q000378:metabolism / Q000473:pathology
chemical_list: D050884:HSP72 Heat-Shock Proteins