Hypothermia triggers iron-dependent lipoperoxidative damage in the isolated rat heart

Franco Magni; Guido Panduri; Nazareno Paolocci

doi:10.1016/0891-5849(94)90124-4

Hypothermia triggers iron-dependent lipoperoxidative damage in the isolated rat heart

Franco Magni, Guido Panduri, Nazareno Paolocci

Research output: Contribution to journal › Article › peer-review

31 Scopus citations

Abstract

The extent and time course of recovery on return to normothermia were studied in isolated rat hearts, perfused with oxygen-saturated Tyrode's solution at 5-7°C. After a 1-h hypothermia period, complete recovery was obtained on rewarming; after 3 h hypothemmia irreversible deterioration of electrical and mechanical activities resulted. The level of lipid peroxidation, evaluated by the thiobarbituric acid (TBA) reaction, showed a dramatic transient increase on return to normothermia, accampanied by a decrease in the levels of reduced glutathione (GSH). Perfusion with iron chelator-containing saline completely prevented both the deterioration and the peak of lipid peroxidation. These results show that lipid peroxidation is responsible for the cold injury. It is proposed that lipid peroxidation is produced as the result of a cold-induced oxidative stress.

Original language	English (US)
Pages (from-to)	465-476
Number of pages	12
Journal	Free Radical Biology and Medicine
Volume	16
Issue number	4
DOIs	https://doi.org/10.1016/0891-5849(94)90124-4
State	Published - Apr 1994
Externally published	Yes

Keywords

Cold injury
Free radicals
Iron chelators
Lipid peroxidation
Myocardium
Rat myocardium

ASJC Scopus subject areas

Biochemistry
Physiology (medical)

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10.1016/0891-5849(94)90124-4

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title = "Hypothermia triggers iron-dependent lipoperoxidative damage in the isolated rat heart",

abstract = "The extent and time course of recovery on return to normothermia were studied in isolated rat hearts, perfused with oxygen-saturated Tyrode's solution at 5-7°C. After a 1-h hypothermia period, complete recovery was obtained on rewarming; after 3 h hypothemmia irreversible deterioration of electrical and mechanical activities resulted. The level of lipid peroxidation, evaluated by the thiobarbituric acid (TBA) reaction, showed a dramatic transient increase on return to normothermia, accampanied by a decrease in the levels of reduced glutathione (GSH). Perfusion with iron chelator-containing saline completely prevented both the deterioration and the peak of lipid peroxidation. These results show that lipid peroxidation is responsible for the cold injury. It is proposed that lipid peroxidation is produced as the result of a cold-induced oxidative stress.",

keywords = "Cold injury, Free radicals, Iron chelators, Lipid peroxidation, Myocardium, Rat myocardium",

author = "Franco Magni and Guido Panduri and Nazareno Paolocci",

note = "Funding Information: Acknowledgements The authors wish to thank Ciba-Geigy (Basel) for the generous gift of Desferal (Desferrioxamine mesylate) and Sclavo (Siena, Italy) for the gift of CPK kit. The technical assistance of S. Pagnotta and M. Valiani is gratefully acknowledged. This work has been funded in part by the Italian Ministry of Education.",

year = "1994",

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doi = "10.1016/0891-5849(94)90124-4",

language = "English (US)",

volume = "16",

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AU - Panduri, Guido

AU - Paolocci, Nazareno

N1 - Funding Information: Acknowledgements The authors wish to thank Ciba-Geigy (Basel) for the generous gift of Desferal (Desferrioxamine mesylate) and Sclavo (Siena, Italy) for the gift of CPK kit. The technical assistance of S. Pagnotta and M. Valiani is gratefully acknowledged. This work has been funded in part by the Italian Ministry of Education.

PY - 1994/4

Y1 - 1994/4

N2 - The extent and time course of recovery on return to normothermia were studied in isolated rat hearts, perfused with oxygen-saturated Tyrode's solution at 5-7°C. After a 1-h hypothermia period, complete recovery was obtained on rewarming; after 3 h hypothemmia irreversible deterioration of electrical and mechanical activities resulted. The level of lipid peroxidation, evaluated by the thiobarbituric acid (TBA) reaction, showed a dramatic transient increase on return to normothermia, accampanied by a decrease in the levels of reduced glutathione (GSH). Perfusion with iron chelator-containing saline completely prevented both the deterioration and the peak of lipid peroxidation. These results show that lipid peroxidation is responsible for the cold injury. It is proposed that lipid peroxidation is produced as the result of a cold-induced oxidative stress.

AB - The extent and time course of recovery on return to normothermia were studied in isolated rat hearts, perfused with oxygen-saturated Tyrode's solution at 5-7°C. After a 1-h hypothermia period, complete recovery was obtained on rewarming; after 3 h hypothemmia irreversible deterioration of electrical and mechanical activities resulted. The level of lipid peroxidation, evaluated by the thiobarbituric acid (TBA) reaction, showed a dramatic transient increase on return to normothermia, accampanied by a decrease in the levels of reduced glutathione (GSH). Perfusion with iron chelator-containing saline completely prevented both the deterioration and the peak of lipid peroxidation. These results show that lipid peroxidation is responsible for the cold injury. It is proposed that lipid peroxidation is produced as the result of a cold-induced oxidative stress.

KW - Cold injury

KW - Free radicals

KW - Iron chelators

KW - Lipid peroxidation

KW - Myocardium

KW - Rat myocardium

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Hypothermia triggers iron-dependent lipoperoxidative damage in the isolated rat heart

Abstract

Keywords

ASJC Scopus subject areas

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