title: [8%-9% and 12%-13% hypoxic gas induced free radicals generation in rat's left and right myocardium].
abstract: Alpha-phenyl-tert-butylnitrone (PBN) was administered intravenously to capture free radicals of rat's myocardium. Rats were exposed to hypoxic gas (8%-9% O2 in N2) for 15 min. The ESR (electron spin resonance) signal intensity of PBN-spin adduct in the left myocardium increased significantly as compared with the normoxia group (n = 5, P < 0.05), but in the right myocardium there was no significant changes between hypoxia and normoxia. Rats exposed to hypoxic gas (12%-13% O2 in N2) were divided into four groups: I (hypoxia for 15 min), II (hypoxia for 60 min), III (hypoxia for 30 min/normoxia for 15 min/hypoxia for 30 min) and IV (injected MPEG- SOD intravenously before hypoxia for 60 min). The ESR signal intensity of PBN-spin adduct of left and right myocardium in group II increased significantly as compared with normoxia group (n = 5, P < 0.01), but the ESR signal intensity of group I didn't show obvious change as compared with normoxia group (n = 5, P > 0.05). In the right myocardium of group III the ESR signal intensity of PBN-spin adduct decreased significantly as compared with group II (n = 5, P < 0.05) and in the left myocardium did not decrease evidently. In the left myocardium of group IV the ESR signal intensity of PBN-spin adduct decreased evidently as compared with group II (n = 5, P < 0.05) and that in the right myocardium did not decrease evidently. When the rats were exposed to 8%-9% hypoxic gas for 15 min and 12%-13% hypoxic gas for 60 min, the SOD (superoxide dismutase, EC 1.11.1.9) activity of myocardium decreased and the content of MDA (malondialdehyde) increased significantly (n = 8, P < 0.05 or P < 0.01). The above results suggested that one way of myocardium free radical gereration may be relevant to decrease of SOD activity. The generation of free radicals pertained chiefly to superoxide free radical in the left myocardium and the membrane structure of myocardium cells might have been damaged largely during hypoxia.
authors.affiliation: Physiological Laboratory of Hypoxia, Shanghai Institute of Physiology, Chinese Academy of Sciences.
authors.forename: Z Y
authors.initials: ZY
authors.lastname: Han
authors.forename: M
authors.initials: M
authors.lastname: Chen
authors.forename: P
authors.initials: P
authors.lastname: Wen
authors.forename: Q H
authors.initials: QH
authors.lastname: Wang
mesh_terms: D000818:Animals; D003497:Cyclic N-Oxides; D004578:Electron Spin Resonance Spectroscopy; D005609:Free Radicals / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D009589:Nitrogen Oxides; D051381:Rats; D017207:Rats, Sprague-Dawley; D013113:Spin Labels; D013482:Superoxide Dismutase / Q000378:metabolism*
chemical_list: D003497:Cyclic N-Oxides; D005609:Free Radicals; D009589:Nitrogen Oxides; D013113:Spin Labels; C029217:phenyl-N-tert-butylnitrone; D008315:Malondialdehyde; D013482:Superoxide Dismutase