| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5902368 | Journal of Diabetes and its Complications | 2015 | 8 Pages |
AimsMyocardial infarction (MI) is a common cause of mortality in patients with diabetes mellitus (DM) and vascular dysfunction is a major component of diabetic cardiomyopathy. We investigated the systemic influence of acute MI on the diabetes-induced pathogenic changes in the rat aorta.MethodsNondiabetic Wistar (W) and type-2 diabetic Goto-Kakizaki (GK) rats underwent 45 min of left anterior descending coronary artery occlusion followed by 24 h of reperfusion. Isometric force was measured using organ bath.ResultsPlasma glucose-levels were significantly higher in diabetic rats (GK + sham: 13 ± 2 mM; GK + MI: 19 ± 2 mM) compared to nondiabetic rats (W + sham: 8 ± 0 mM; W + MI: 8 ± 1 mM). Acetylcholine-induced relaxation was significantly weaker in rings from W + MI and GK + MI rats compared to corresponding sham-operated animals. Myocardial reperfusion injury was smaller in GK + MI than W + MI rats, and the concentration-response curves to acetylcholine were significantly enhanced in rings from GK + MI than W + MI rats. Nevertheless, the relaxation response to acetylcholine was similar in W + sham and GK + sham. Densitometric analysis of bands for endothelial nitric oxide synthase showed a significant decrease in W + MI rats compared to W + sham and GK + sham animals. Aortas from both GK + sham and GK + MI rats showed impaired contractile responses to phenylephrine in comparison with the nondiabetics.ConclusionsFor the first time we showed that short-term and mild type-2 DM improved remote endothelial dysfunction after reperfused acute MI.
