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
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