HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/E629    most recent 00221.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Su, H. Articles by Gao, F. Search for Related Content PubMed PubMed Citation Articles by Su, H. Articles by Gao, F.

Acute hyperglycemia exacerbates myocardial ischemia/reperfusion injury and blunts cardioprotective effect of GIK

Departments of ¹Cardiology, ²Geriatrics, ³Pediatrics, Xijing Hospital, and ⁴Physiology, Fourth Military Medical University, Xi'an, China

Submitted 9 April 2007 ; accepted in final form 16 May 2007

There is a close association between hyperglycemia and increased risk of mortality after acute myocardial infarction (AMI). However, whether acute hyperglycemia exacerbates myocardial ischemia/reperfusion (MI/R) injury remains unclear. We observed the effects of acute hyperglycemia on MI/R injury and on the cardioprotective effect of glucose-insulin-potassium (GIK). Male rats were subjected to 30 min of myocardial ischemia and 6 h of reperfusion. Rats were randomly received one of the following treatments (at 4 ml·kg^–1·h^–1 iv): Vehicle, GIK (GIK during reperfusion; glucose: 200g/l, insulin: 60 U/l, KCL: 60 mmol/l), HG (high glucose during ischemia; glucose:500 g/l), GIK + HG (HG during I and GIK during R) or GIK + wortmannin (GIK during R and wortmannin 15 min before R). Blood glucose, plasma insulin concentration and left ventricular pressure (LVP) were monitored throughout the experiments. Hyperglycemia during ischemia not only significantly increased myocardial apoptosis (23.6 ± 1.7% vs. 18.8 ± 1.4%, P < 0.05 vs. vehicle), increased infarct size (IS) (45.6 ± 3.0% vs. 37.6 ± 2.0%, P < 0.05 vs. vehicle), decreased Akt and GSK-3 phosphorylations (0.5 ± 0.2 and 0.6 ± 0.1% fold of vehicle, respectively, P < 0.05 vs. vehicle) following MI/R, but almost completely blocked the cardioprotective effect afforded by GIK, as evidenced by significantly increased apoptotic index (19.1 ± 2.0 vs. 10.3 ± 1.2%, P < 0.01 vs. GIK), increased myocardial IS (39.2 ± 2.8 vs. 27.2 ± 2.1%, P < 0.01 vs. GIK), decreased Akt phosphorylation (1.1 ± 0.1 vs. 1.7 ± 0.2%, P < 0.01 vs. GIK) and GSK-3 phosphorylation (1.4 ± 0.2 vs. 2.3 ± 0.2%, P < 0.05 vs. GIK). Hyperglycemia significantly exacerbates MI/R injury and blocks the cardioprotective effect afforded by GIK, which is, at least in part, due to hyperglycemia-induced decrease of myocardial Akt activation.

Akt; glucose-insulin-potassium

This article has been cited by other articles:

				M. Gandhi, B. A. Finegan, and A. S. Clanachan Role of glucose metabolism in the recovery of postischemic LV mechanical function: effects of insulin and other metabolic modulators Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2576 - H2586. [Abstract] [Full Text] [PDF]