Ischemic and reperfusion injury of cyanotic myocardium in chronic hypoxic rat model: Changes in cyanotic myocardial antioxidant system

K. Nakanishi, M. Inoue, E. Sugawara, S. Sano

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Objective: The objective was to evaluate the effect of left ventricular function on cyanotic myocardium after ischemia-reperfusion and to determine the effect of cyanosis on the myocardial antioxidant system. Methods: Cyanotic hearts (cyanotic group) were obtained from rats housed in a hypoxic chamber (10% oxygen) for 2 weeks and control hearts (control group) from rats maintained in ambient air. Isolated, crystalloid perfused working hearts were subjected to 15 minutes of global normothermic ischemia and 20 minutes of reperfusion, and functional recovery was evaluated in the two groups. Myocardial superoxide dismutase, glutathione peroxidase, glutathione reductase activity, and reduced glutathione content were measured separately in the cytoplasm and mitochondria at the end of the preischemic, ischemic, and reperfusion periods. Results: Mean cardiac output/left ventricular weight was not significantly different between the two groups. Percent recovery of cardiac output was significantly lower in the cyanotic group than in the control group (56.1% ± 5.7% vs 73.0% ± 3.1%, p = 0.001). Mitochondrial superoxide dismutase, mitochondrial and cytosolic glutathione reductase activity, and cytosolic reduced glutathione were significantly lower in the cyanotic group than in the control group at end-ischemia (superoxide dismutase, 3.7 ± 1.3 vs 5.9 ± 1.5 units/mg protein, p = 0.012; mitochondrial glutathione reductase, 43.7 ± 14.0 vs 71.0 ± 30.3 munits/mg protein, p = 0.039; cytosolic glutathione reductase, 13.7 ± 2.0 vs 23.2 ± 4.2 munits/mg protein, p <0.001; and reduced glutathione, 0.69 ± 0.10 vs 0.91 ± 0.24 μg/mg protein, p = 0.037). Conclusions: Cyanosis impairs postischemic functional recovery and depresses myocardial antioxidant reserve during ischemia. Reduced antioxidant reserve at end-ischemia may result in impaired postischemic functional recovery of cyanotic myocardium.

Original languageEnglish
Pages (from-to)1088-1096
Number of pages9
JournalJournal of Thoracic and Cardiovascular Surgery
Volume114
Issue number6
DOIs
Publication statusPublished - 1997

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Reperfusion Injury
Glutathione Reductase
Myocardium
Ischemia
Antioxidants
Superoxide Dismutase
Reperfusion
Glutathione
Cyanosis
Cardiac Output
Control Groups
Proteins
Glutathione Peroxidase
Left Ventricular Function
Mitochondria
Cytoplasm
Air
Oxygen
Weights and Measures

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Ischemic and reperfusion injury of cyanotic myocardium in chronic hypoxic rat model : Changes in cyanotic myocardial antioxidant system. / Nakanishi, K.; Inoue, M.; Sugawara, E.; Sano, S.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 114, No. 6, 1997, p. 1088-1096.

Research output: Contribution to journalArticle

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title = "Ischemic and reperfusion injury of cyanotic myocardium in chronic hypoxic rat model: Changes in cyanotic myocardial antioxidant system",
abstract = "Objective: The objective was to evaluate the effect of left ventricular function on cyanotic myocardium after ischemia-reperfusion and to determine the effect of cyanosis on the myocardial antioxidant system. Methods: Cyanotic hearts (cyanotic group) were obtained from rats housed in a hypoxic chamber (10{\%} oxygen) for 2 weeks and control hearts (control group) from rats maintained in ambient air. Isolated, crystalloid perfused working hearts were subjected to 15 minutes of global normothermic ischemia and 20 minutes of reperfusion, and functional recovery was evaluated in the two groups. Myocardial superoxide dismutase, glutathione peroxidase, glutathione reductase activity, and reduced glutathione content were measured separately in the cytoplasm and mitochondria at the end of the preischemic, ischemic, and reperfusion periods. Results: Mean cardiac output/left ventricular weight was not significantly different between the two groups. Percent recovery of cardiac output was significantly lower in the cyanotic group than in the control group (56.1{\%} ± 5.7{\%} vs 73.0{\%} ± 3.1{\%}, p = 0.001). Mitochondrial superoxide dismutase, mitochondrial and cytosolic glutathione reductase activity, and cytosolic reduced glutathione were significantly lower in the cyanotic group than in the control group at end-ischemia (superoxide dismutase, 3.7 ± 1.3 vs 5.9 ± 1.5 units/mg protein, p = 0.012; mitochondrial glutathione reductase, 43.7 ± 14.0 vs 71.0 ± 30.3 munits/mg protein, p = 0.039; cytosolic glutathione reductase, 13.7 ± 2.0 vs 23.2 ± 4.2 munits/mg protein, p <0.001; and reduced glutathione, 0.69 ± 0.10 vs 0.91 ± 0.24 μg/mg protein, p = 0.037). Conclusions: Cyanosis impairs postischemic functional recovery and depresses myocardial antioxidant reserve during ischemia. Reduced antioxidant reserve at end-ischemia may result in impaired postischemic functional recovery of cyanotic myocardium.",
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AB - Objective: The objective was to evaluate the effect of left ventricular function on cyanotic myocardium after ischemia-reperfusion and to determine the effect of cyanosis on the myocardial antioxidant system. Methods: Cyanotic hearts (cyanotic group) were obtained from rats housed in a hypoxic chamber (10% oxygen) for 2 weeks and control hearts (control group) from rats maintained in ambient air. Isolated, crystalloid perfused working hearts were subjected to 15 minutes of global normothermic ischemia and 20 minutes of reperfusion, and functional recovery was evaluated in the two groups. Myocardial superoxide dismutase, glutathione peroxidase, glutathione reductase activity, and reduced glutathione content were measured separately in the cytoplasm and mitochondria at the end of the preischemic, ischemic, and reperfusion periods. Results: Mean cardiac output/left ventricular weight was not significantly different between the two groups. Percent recovery of cardiac output was significantly lower in the cyanotic group than in the control group (56.1% ± 5.7% vs 73.0% ± 3.1%, p = 0.001). Mitochondrial superoxide dismutase, mitochondrial and cytosolic glutathione reductase activity, and cytosolic reduced glutathione were significantly lower in the cyanotic group than in the control group at end-ischemia (superoxide dismutase, 3.7 ± 1.3 vs 5.9 ± 1.5 units/mg protein, p = 0.012; mitochondrial glutathione reductase, 43.7 ± 14.0 vs 71.0 ± 30.3 munits/mg protein, p = 0.039; cytosolic glutathione reductase, 13.7 ± 2.0 vs 23.2 ± 4.2 munits/mg protein, p <0.001; and reduced glutathione, 0.69 ± 0.10 vs 0.91 ± 0.24 μg/mg protein, p = 0.037). Conclusions: Cyanosis impairs postischemic functional recovery and depresses myocardial antioxidant reserve during ischemia. Reduced antioxidant reserve at end-ischemia may result in impaired postischemic functional recovery of cyanotic myocardium.

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