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Off‐Pump Glutamate Pre‐ and Post‐Conditioning against an Acute Myocardial Infarction: Role of ATP‐Sensitive Potassium Channels
Author(s) -
AbdEfattah Anwar Saad,
Guo JianHua,
Goa ShinPing,
Mahgoub Mahmoud Ahmed
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1033.22
Subject(s) - myocardial infarction , cardiology , potassium channel , glutamate receptor , potassium , medicine , conditioning , chemistry , pharmacology , receptor , statistics , mathematics , organic chemistry
Background Metabotropic glutamate receptor 5(mGluR5) is expressed in hearts. We determined whether infusion of glutamate (GLU) pre‐ (PreC) and post‐conditions (Post‐C) against acute myocardial infarction (MI) and if mitochondrial (Mito) K ATP channel is involved (using 5‐Hydroxydecanoate). Methods Anesthetized dogs (n = 46), instrumented to monitor LV contractility using sonomicrometry, subjected to 90 minutes LAD coronary artery occlusion and 4 hrs reperfusion (Rep). Dogs were infused with 50ml of vehicle (control), glutamate (Glu100μmol/L) or 5HD (5 mg/Kg)+GLU before ischemia (PreC) or before Rep (PostC). Coronary blood flow was measured using colored microspheres. LV function (stroke work/end diastolic relationships) was determined. The infarct size and LV and risk areas were measured. Four animals were excluded. Data were analyzed by ANOVA and presented as mean± SEM (n = 6). Results LV function significantly recovered in Glu‐treated groups (p=NS vs., baseline, p < 0.05 vs. control, 5HD). Poor LV functional recovery was seen in the control (36.2±5%) and 5HD (46.1±6%)groups (p < 0.05 vs Glu groups). GLU reduced the infarct size (38.2±6% in the control group to11.1±4% and 14.3±3 in GLU PreC and PostC groups. 5‐HD abolished Glu‐infarct size limitation. Conclusions Infusion of GLU pre‐ and post‐conditions the myocardium against INF. Mito‐K ATP channels are involved in GLU‐mediated cardioprotection.