Electrolysis-induced myocardial dysfunction: A novel method for the study of free radical mediated tissue injury
- 31 July 1986
- journal article
- Published by Elsevier BV in Journal of Pharmacological Methods
- Vol. 15 (4), 305-320
- https://doi.org/10.1016/0160-5402(86)90010-0
Abstract
Oxygen-derived free radicals and other oxidizing species are thought to be involved in inflammation and ischemic tissue injuries. Recently, oxygen-derived free radicals also have been implicated in tissue injury of the myocardium subjected to ischemia/reperfusion. The purpose of this investigation was to determine if electrolysis of a physiological buffer would serve as a source of free radicals, and if these radicals would lead to alterations in myocardial function. Isolated Langendorff-perfused rabbit hearts perfused with buffer subjected to a 20 mA D.C. current for 2 min demonstrated significant increases in coronary perfusion pressure (37 ± 6 mmHg), left ventricular end diastolic pressure (41 ± 7 mmHg), and loss in left ventricular developed pressure (35 ± 5%). The free radical scavengers, Superoxide dismutase and a combination of tryptophan plus glycine, were effective in protecting the hearts from the effects of electrolysis. The presence of free radicals was semiquantitated with a radical-luminol chemiluminescent assay. In this assay a variety of radical scavengers and antioxidants were effective (i.e., dimethyl sulfoxide, nitro blue tetrazolium, ascorbate, superoxide dismutase, 1, 3-diphenyisobenzofuran, and glycine, catalase), whereas mannitol and tryptophan were not effective. The data indicate that electrolysis of a physiological buffer produces a milieu containing several reactive oxygen species or free radicals that have the potential to produce alterations in a biological system. This method has the advantage over existing protocols for the generation of radicals in that it is a blood-free and an enzyme-free system.Keywords
This publication has 11 references indexed in Scilit:
- The independent effects of oxygen radical scavengers on canine infarct size. Reduction by superoxide dismutase but not catalase.Circulation Research, 1985
- Canine myocardial reperfusion injury. Its reduction by the combined administration of superoxide dismutase and catalase.Circulation Research, 1984
- Free radical mediation of the effects of acidosis on calcium transport by cardiac sarcoplasmic reticulum in whole heart homogenatesCardiovascular Research, 1984
- Chemiluminescence and Superoxide Anion Production by Leukocytes from Diabetic Patients*Journal of Clinical Endocrinology & Metabolism, 1983
- Lipid Peroxidation and Acute Myocardial IschemiaAdvances in experimental medicine and biology, 1983
- Role of free radicals in catecholamine-induced cardiomyopathyCanadian Journal of Physiology and Pharmacology, 1982
- The role of lipid peroxidation in pathogenesis of ischemic damage and the antioxidant protection of the heartBasic Research in Cardiology, 1982
- The role of superoxide anion in peroxidase-catalyzed chemiluminescence of luminolArchives of Biochemistry and Biophysics, 1982
- Chemiluminescent measurement of free radicals and antioxidant molecular-protection inside living rat-mitochondriaExperimental Gerontology, 1980
- Role of a peroxide intermediate in the chemiluminescence of luminol. A mechanistic studyJournal of the American Chemical Society, 1980