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Maulik N, Watanabe M, Engelman D, et al. Myocardial adaptation to ischemia by oxidative stress induced by endotoxin. Am J Physiol. 1995;269(4):C907-16doi: 10.1152/ajpcell.1995.269.4.C907.
Maulik, N., Watanabe, M., Engelman, D., Engelman, R. M., Kagan, V. E., Kisin, E., Tyurin, V., Cordis, G. A., & Das, D. K. (1995). Myocardial adaptation to ischemia by oxidative stress induced by endotoxin. The American journal of physiology, 269(4), C907-16. https://doi.org/10.1152/ajpcell.1995.269.4.C907
Maulik, N, et al. "Myocardial adaptation to ischemia by oxidative stress induced by endotoxin." The American journal of physiology vol. 269,4 (1995): C907-16. doi: https://doi.org/10.1152/ajpcell.1995.269.4.C907
Maulik N, Watanabe M, Engelman D, Engelman RM, Kagan VE, Kisin E, Tyurin V, Cordis GA, Das DK. Myocardial adaptation to ischemia by oxidative stress induced by endotoxin. Am J Physiol. 1995 Oct;269(4):C907-16. doi: 10.1152/ajpcell.1995.269.4.C907. PMID: 7485460.
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Am J Physiol. 1995 Oct;269(4):C907-16. doi: 10.1152/ajpcell.1995.269.4.C907.

Myocardial adaptation to ischemia by oxidative stress induced by endotoxin.

The American journal of physiology

N Maulik, M Watanabe, D Engelman, R M Engelman, V E Kagan, E Kisin, V Tyurin, G A Cordis, D K Das

Affiliations

  1. Department of Surgery, University of Connecticut School of Medicine, Farmington 06030, USA.

PMID: 7485460 DOI: 10.1152/ajpcell.1995.269.4.C907

Abstract

In this study, we examined the effects of oxidative stress adaptation on myocardial ischemic reperfusion injury. Oxidative stress was induced by injecting endotoxin (0.5 mg/kg) into the rat. After 24 h, rats were killed, hearts were isolated, and the effects of ischemia-reperfusion were studied using an isolated working heart preparation. The development of oxidative stress was examined by assessing malonaldehyde production in the heart. The antioxidant defense system was studied by estimating antioxidant enzyme activities and ascorbate- as well as thiol-dependent antioxidant reserve. The results of our study indicated that endotoxin induced oxidative stress within 1 h of treatment; the stress was reduced progressively and steadily up to 24 h. The antioxidant enzymes superoxide dismutase, catalase, glutathione (GSH) peroxidase, and GSH reductase were lowered up to 2 h and then increased. Both thiol- and ascorbate-dependent antioxidant reserve were enhanced, but the enhancement of the former was only transitory. After 24 h, endotoxin provided adequate protection to the heart from the ischemic-reperfusion injury, as evidenced by improved left ventricular function and aortic flow. Our results suggest that the induction of oxidative stress by endotoxin-induced adaptive modification of the antioxidant defense in the heart, thereby reducing ischemic-reperfusion injury.

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