Changes in Energy Levels by Dexamethasone in Ischemic Hearts and Brains in Male Mice.

Abstract:

BACKGROUND:Glucocorticoids have been shown to alleviate ischemia-induced myocardial injury, while aggravating neuronal damage caused by ischemia. As energy failure is a predominant factor in cellular viability, we examined the effects of glucocorticoids on energy utilization in the mouse heart and brain. METHODS:Seventy-two male ddY mice were assigned to 1 of 3 groups: saline (S), dexamethasone (a glucocorticoid without mineralocorticoid activity, 5 mg/kg) (D), and metyrapone (a potent inhibitor of the synthesis of glucocorticoids, 100 mg/kg) (M) groups (n=24 in each). Three hours after intraperitoneal administration, all animals were decapitated, and the heads were frozen in liquid nitrogen after 0, 0.5, 1, or 2 minutes (n=6 in each). The hearts were immediately removed and frozen in liquid nitrogen after 0, 5, 10, or 20 minutes of incubation at 37°C (n=6 in each). The concentrations of adenylates and monoamines were determined by high-performance liquid chromatography. RESULTS:In the heart, the adenosine 5'-triphosphate (ATP) concentration did not differ among the 3 groups at 0 minute of ischemia (3 h of S, D, or M treatment). Ischemia for 5 minutes decreased the ATP content to 21% of the basal level in the S group. The ATP decrease was suppressed by either the D or M treatment, such that after 5 minutes ATP levels were 63% and 64% of each basal level, respectively. In the brain, the ATP level in the M group was 62% of that in the S group at 0 minute of ischemia, and the 5'-monophosphate (AMP) level was 276% of that in the S group. Brain dopamine metabolism was facilitated by dexamethasone, and suppressed by metyrapone. CONCLUSIONS:The relationship between effects of glucocorticoids on ischemia-induced changes in energy levels and cellular viability was not clearly elucidated.

authors

Yorozuya T,Namba C,Adachi N,Nakanishi K,Dote K,Nagaro T

doi

10.1097/ANA.0000000000000153

subject

Has Abstract

pub_date

2015-10-01 00:00:00

pages

295-303

issue

4

eissn

0898-4921

issn

1537-1921

journal_volume

27

pub_type

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