title: Hemoglobin vesicle improves recovery of cardiac function after ischemia-reperfusion by attenuating oxidative stress in isolated rat hearts.
abstract: Hemoglobin vesicle (HbV) could be a useful blood substitute in emergency medicine. The aim of this study was to clarify the effects of HbV on cardiac function after ischemia-reperfusion (I/R) ex vivo. Isolated rat hearts were perfused according to the Langendorff method. An ischemia-reperfusion group (n = 6) was subjected to 25 minutes of global ischemia and 30 minutes of reperfusion. HbV (hemoglobin, 0.33 g/dL) was perfused before ischemia-reperfusion for 10 minutes (HbV group, n = 6). Hemodynamics were monitored, and tissue glutathione contents were measured. The redox state of reactive thiols in cardiac tissues was assessed by the biotinylated iodoacetamide labeling method. Left ventricular developed pressure was significantly recovered in the HbV group after 30 minutes of reperfusion (56.3 ± 2.8 mm Hg vs. ischemia-reperfusion group 27.0 ± 8.0 mm Hg, P < 0.05). Hemodynamic changes induced by HbV were similar to those observed when N-nitro-L-arginine methyl ester was perfused for 10 minutes before ischemia-reperfusion (L-NAME group). The oxidized glutathione contents of cardiac tissues significantly decreased, and biotinylated iodoacetamide labeling of thiols was maintained in both the HbV and the L-NAME groups. HbV improved the recovery of cardiac function after ischemia-reperfusion in isolated rat hearts. This mechanism is dependent on functional protection against thiol oxidation.
authors.affiliation: First Department of Internal Medicine, National Defense Medical College, Saitama, Japan.
authors.forename: Jun
authors.initials: J
authors.lastname: Nakajima
authors.forename: Motoaki
authors.initials: M
authors.lastname: Bessho
authors.forename: Takeshi
authors.initials: T
authors.lastname: Adachi
authors.forename: Tadashi
authors.initials: T
authors.lastname: Yamagishi
authors.forename: Shinichi
authors.initials: S
authors.lastname: Tokuno
authors.forename: Hirohisa
authors.initials: H
authors.lastname: Horinouchi
authors.forename: Fumitaka
authors.initials: F
authors.lastname: Ohsuzu
mesh_terms: D000818:Animals; D001802:Blood Substitutes / Q000494:pharmacology / Q000627:therapeutic use*; D002374:Catalase / Q000378:metabolism; D003326:Coronary Circulation / Q000187:drug effects / Q000502:physiology; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology / Q000627:therapeutic use; D010084:Oxidation-Reduction / Q000187:drug effects; D018384:Oxidative Stress / Q000187:drug effects*; D010477:Perfusion; D011506:Proteins / Q000378:metabolism; D019289:Pyruvic Acid / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D053835:Unilamellar Liposomes; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000517:prevention & control
chemical_list: D001802:Blood Substitutes; D011506:Proteins; D013438:Sulfhydryl Compounds; D053835:Unilamellar Liposomes; D019344:Lactic Acid; D019289:Pyruvic Acid; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005978:Glutathione; D019803:Glutathione Disulfide; D019331:NG-Nitroarginine Methyl Ester