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  • Title: Cardiac tissue iron: effects on post-ischemic function and free radical production, and its possible role during preconditioning.
    Author: Kramer JH, Lightfoot FG, Weglicki WB.
    Journal: Cell Mol Biol (Noisy-le-grand); 2000 Dec; 46(8):1313-27. PubMed ID: 11156477.
    Abstract:
    We determined whether prior treatment of rats (study 1) with subthreshold doses of iron (no evidence of cardiac tissue overload), or in vitro ischemic pre-conditioning (IP: 5 min. Ischemia (I)/5 min. Reperfusion (R) x 2 cycles) of hearts from untreated rats (study 2), can modulate redox-active cardiac tissue iron levels or distribution, leading to alterations in post-ischemic lipid peroxidation-derived free radical (FR) production and severity of reperfusion injury. In study 1, rats received biweekly i.p. injections of 0 (saline=S), 3, 6, or 12 mg FeCl3/ml for 3-wks prior to imposing 30 min. I/15 min. R in vitro. The highest dose caused no elevations in plasma or heart tissue Fe levels, but did further reduce post-ischemic recoveries of left ventricular developed pressure (17% lower), cardiac work (57%) and output (54%), and increased effluent lipid hydroperoxides (2.1-fold) compared to the S-group. Post-ischemic FR production was assessed in toluene-extracted effluent by ESR spectroscopy and alpha-phenyl-N-tert butylnitrone (PBN=2.5 mM perfusate) spin trapping. PBN/alkoxyl (alphaH=1.90 G, alphaN=13.63 G) was the dominant signal detected in all groups; however, Fe-treated groups displayed significant dose-dependent increases in total alkoxyl content (3, 6, 12 mg/ml: 1.8-, 2.3-, 2.7-fold higher) compared to the S-group. These data suggest that even mild, non-overloading doses of iron can be functionally and oxidatively detrimental to hearts when an I/R stress is imposed. In study 2, isolated hearts from untreated rats were exposed to two-IP cycles: during IP, total effluent iron content (atomic absorption) increased 11.4-fold compared to control and analysis of cardiovascular tissue iron distribution (X-ray microanalysis) suggested that iron loss from capillary endothelium was far greater than from tissue myocytes. Moreover, iron-catalyzed production of alkoxyl radicals following severe I/R stress (40 min. I/15 min. R) was substantially lower (73%) in IP hearts compared to the non-IP counterparts. These preliminary findings suggest that cardioprotection resulting from IP may, in part, be related to IP-induced release of cardiovascular endothelial iron (redox-active) prior to imposing severe I/R stress.
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