Title of article :
Improved Myocardial Tolerance to Ischaemia in the Diabetic Rabbit
Author/Authors :
Guylaine Hadour، نويسنده , , René Ferrera، نويسنده , , Laurent Sebbag، نويسنده , , Rémi Forrat، نويسنده , , Jacques Delaye، نويسنده , , Michel de Lorgeril، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1998
Pages :
7
From page :
1869
To page :
1875
Abstract :
Because cardiac complications after myocardial infarction are more frequent in diabetics, we tested whether experimentally-induced diabetes may increase ischaemic myocardial injury in 23 rabbits. Diabetes was induced in randomized rabbits with the alloxan method. After 2 months, diabetic rabbits underwent a 30-min coronary occlusion followed by 3-h reperfusion and were compared with controls. Collateral flow was measured by the radioactive microsphere technique and infarct size by tetrazolium staining. Infarct size represented 28.6±4% of area-at-risk in controls and 16.5±3% in diabetics (P<0.05). Collateral flow (0.06±0.03 ml/min/g in controls and 0.014±0.004 ml/min/g in diabetics) and area-at-risk (50.2±4.2% of left ventricle in controls and 53.9±5.4% in diabetics) were similar in both groups. There was a significant positive correlation between area-at-risk and infarct size in both groups (r=0.60 and 0.70, respectively) and for a given area-at-risk, diabetic rabbits developed smaller myocardial infarction than controls (covariance analysis,P<0.01). In additional experiments, hyperglycemia induced by intravenous glucose infusion in non-diabetic rabbits did not protect the ischaemic myocardium (infarct size: 37.9±12.5%). In conclusion, diabetes in the rabbit induces a chronic and metabolic form of preconditioning. Further studies are needed to explore the mechanism and time course of this protection.
Keywords :
Myocardial infarction , Preconditioning , Collateral flow , Diabetes , Rabbit.
Journal title :
Journal of Molecular and Cellular Cardiology
Serial Year :
1998
Journal title :
Journal of Molecular and Cellular Cardiology
Record number :
526062
Link To Document :
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