IMPROVED MYOCARDIAL TOLERANCE TO ISCHEMIA IN THE DIABETIC RABBIT

Citation
G. Hadour et al., IMPROVED MYOCARDIAL TOLERANCE TO ISCHEMIA IN THE DIABETIC RABBIT, Journal of Molecular and Cellular Cardiology, 30(9), 1998, pp. 1869-1875
Citations number
34
Categorie Soggetti
Cardiac & Cardiovascular System","Cell Biology
ISSN journal
00222828
Volume
30
Issue
9
Year of publication
1998
Pages
1869 - 1875
Database
ISI
SICI code
0022-2828(1998)30:9<1869:IMTTII>2.0.ZU;2-N
Abstract
Because cardiac complications after myocardial infarction are more fre quent in diabetics, we tested whether experimentally-induced diabetes may increase ischaemic myocardial injury in 23 rabbits, Diabetes was i nduced 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 Row was measu red by the radioactive microsphere technique and infarct size by tetra zolium 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 diabe tics) and area-at-risk: (50.2 +/- 4.2% of left ventricle in controls a nd 53.9 +/- 5.4% in diabetics) were similar in both groups. There was a significant positive correlation between area-at-risk and infarct si ze in both groups (r = 0.60 and 0.70, respectively) and for a given ar ea-at-risk, diabetic rabbits developed smaller myocardial infarction t han 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 an d metabolic form of preconditioning. Further studies are needed to exp lore the mechanism and time course of this protection. (C) 1998 Academ ic Press