TY - JOUR
T1 - Greater susceptibility of failing cardiac myocytes to oxygen free radical-mediated injury
AU - Tsutsui, Hiroyuki
AU - Ide, Tomomi
AU - Hayashidani, Shunji
AU - Suematsu, Nobuhiro
AU - Utsumi, Hideo
AU - Nakamura, Ryo
AU - Egashira, Kensuke
AU - Takeshita, Akira
N1 - Funding Information:
This work is supported in part by grants from the Ministry of Education, Science and Culture (No. 07266220, 08258221, 09670724). Presented in part at the 72nd Scientific Session of the American Heart Association, Atlanta, Georgia, November 7–10, 1999 and published in abstract form (Circulation 1999; 100:I–410).
PY - 2001
Y1 - 2001
N2 - Objective: Oxygen-derived free radicals can produce myocardial cellular damage, which might contribute to the ischemia-reperfusion injury and to heart failure (HF). However, the effects of oxygen radicals on myocyte structure have not been examined in the failing heart. Methods: We examined the susceptibility of intact cardiac myocytes isolated from control (n=16) and rapid pacing (240 bpm, 4 wks)-induced HF (n=8) dog hearts to an exogenous hydroxyl radical (·OH), generated from H2O2 and Fe3+-nitrilotriacetate. The production of ·OH was monitored by electron spin resonance with 5,5'-dimethyl-1-pyroline-N-oxide (DMPO) as a spin trap. Results: The magnitude of DMPO-OH signals was not attenuated in the presence of either control or HF myocytes. ·OH induced a time-dependent decrease in myocyte length (i.e. hypercontracture). The time to the onset of hypercontracture and that to the submaximal hypercontracture after exposure was significantly shortened in HF. Activities of superoxide dismutase, catalase, and glutathione peroxidase was not decreased in HF. Conclusions: HF myocytes were more susceptible to oxidative stress-induced cellular injury, which was not due to decreased antioxidant defense, but to the intrinsic properties of cells. (C) 2001 Elsevier Science B.V.
AB - Objective: Oxygen-derived free radicals can produce myocardial cellular damage, which might contribute to the ischemia-reperfusion injury and to heart failure (HF). However, the effects of oxygen radicals on myocyte structure have not been examined in the failing heart. Methods: We examined the susceptibility of intact cardiac myocytes isolated from control (n=16) and rapid pacing (240 bpm, 4 wks)-induced HF (n=8) dog hearts to an exogenous hydroxyl radical (·OH), generated from H2O2 and Fe3+-nitrilotriacetate. The production of ·OH was monitored by electron spin resonance with 5,5'-dimethyl-1-pyroline-N-oxide (DMPO) as a spin trap. Results: The magnitude of DMPO-OH signals was not attenuated in the presence of either control or HF myocytes. ·OH induced a time-dependent decrease in myocyte length (i.e. hypercontracture). The time to the onset of hypercontracture and that to the submaximal hypercontracture after exposure was significantly shortened in HF. Activities of superoxide dismutase, catalase, and glutathione peroxidase was not decreased in HF. Conclusions: HF myocytes were more susceptible to oxidative stress-induced cellular injury, which was not due to decreased antioxidant defense, but to the intrinsic properties of cells. (C) 2001 Elsevier Science B.V.
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U2 - 10.1016/S0008-6363(00)00197-8
DO - 10.1016/S0008-6363(00)00197-8
M3 - Article
C2 - 11121801
AN - SCOPUS:0034749689
VL - 49
SP - 103
EP - 109
JO - Cardiovascular Research
JF - Cardiovascular Research
SN - 0008-6363
IS - 1
ER -