Chronic corticosterone treatment increases myocardial infarct size in rats with ischemia-reperfusion injury

Deborah A. Scheuer, Steve Wayne Mifflin

Research output: Contribution to journalArticle

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Abstract

Experiments were conducted to determine the effect of chronic elevations in corticosterone on myocardial infarct size. Male Sprague-Dawley rats were treated for 7-22 days with corticosterone. Plasma corticosterone concentrations averaged 0.8 ± 0.3 in control and 14.9 ± 1.2 μg/dl in corticosterone-treated conscious rats. Experiments were performed in anesthetized rats. After a 30-min control period, myocardial ischemia (30 min)-reperfusion (3 h) was performed in control and corticosterone-treated rats. Mean arterial pressure (± SE) in control rats during control, ischemia, and reperfusion periods averaged 111 ± 4,100 ± 5, and 94 ± 4 mniHg (n = 6), respectively. Chronic treatment with corticosterone increased mean arterial pressure in all three periods (128 ± 6, 117 ± 7, and 109 ± 7 mmHg; n = 8; P < 0.05). Infarct size (as % area at risk) was significantly larger in rats with chronic elevations in corticosterone compared with control rats (77 ± 2 vs. 51 ± 5%; P < 0.05). Acute (2 h) blockade of the glucocorticoid type II receptors with mifepristone antagonized the increases in arterial pressure and infarct size produced by chronic administration of corticosterone. Neither mifepristone nor acutely administered corticosterone affected arterial pressure or infarct size in rats without chronic corticosterone treatment. The effect of chronic elevations in plasma corticosterone concentration to increase infarct size could contribute to the increased risk of cardiovascular disease in clinical conditions associated with elevated glucocorticoid levels.

Original languageEnglish
JournalAmerican Journal of Physiology
Volume272
Issue number6 PART 2
StatePublished - 1 Dec 1997

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Corticosterone
Reperfusion Injury
Myocardial Infarction
Arterial Pressure
Mifepristone
Reperfusion
Glucocorticoid Receptors
Glucocorticoids
Myocardial Ischemia
Sprague Dawley Rats
Cardiovascular Diseases
Ischemia

Keywords

  • Arterial pressure
  • Glucocorticoids
  • Mifepristone
  • RU-486

Cite this

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title = "Chronic corticosterone treatment increases myocardial infarct size in rats with ischemia-reperfusion injury",
abstract = "Experiments were conducted to determine the effect of chronic elevations in corticosterone on myocardial infarct size. Male Sprague-Dawley rats were treated for 7-22 days with corticosterone. Plasma corticosterone concentrations averaged 0.8 ± 0.3 in control and 14.9 ± 1.2 μg/dl in corticosterone-treated conscious rats. Experiments were performed in anesthetized rats. After a 30-min control period, myocardial ischemia (30 min)-reperfusion (3 h) was performed in control and corticosterone-treated rats. Mean arterial pressure (± SE) in control rats during control, ischemia, and reperfusion periods averaged 111 ± 4,100 ± 5, and 94 ± 4 mniHg (n = 6), respectively. Chronic treatment with corticosterone increased mean arterial pressure in all three periods (128 ± 6, 117 ± 7, and 109 ± 7 mmHg; n = 8; P < 0.05). Infarct size (as {\%} area at risk) was significantly larger in rats with chronic elevations in corticosterone compared with control rats (77 ± 2 vs. 51 ± 5{\%}; P < 0.05). Acute (2 h) blockade of the glucocorticoid type II receptors with mifepristone antagonized the increases in arterial pressure and infarct size produced by chronic administration of corticosterone. Neither mifepristone nor acutely administered corticosterone affected arterial pressure or infarct size in rats without chronic corticosterone treatment. The effect of chronic elevations in plasma corticosterone concentration to increase infarct size could contribute to the increased risk of cardiovascular disease in clinical conditions associated with elevated glucocorticoid levels.",
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Chronic corticosterone treatment increases myocardial infarct size in rats with ischemia-reperfusion injury. / Scheuer, Deborah A.; Mifflin, Steve Wayne.

In: American Journal of Physiology, Vol. 272, No. 6 PART 2, 01.12.1997.

Research output: Contribution to journalArticle

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AU - Scheuer, Deborah A.

AU - Mifflin, Steve Wayne

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