Changes in vasodilation following myocardial ischemia/reperfusion in rats

- Carbachol and ADPβS were both 100% dependent on NO in arteries from sham animals.
- In contrast to ADPβS, Carbachol induced dilation was sensitive to depolarization.
- Endothelial NO dependent ADPβS signalling, was significantly reduced after I/R.
- Following I/R, an H2O2 dependent EDH occurs in response to carbachol and ADPβS.
- Calcitonin gene-related peptide induced vasodilation was also reduced after I/R.

BackgroundBlockage of a coronary artery, usually caused by arteriosclerosis, can lead to life threatening acute myocardial infarction. Opening with PCI (percutaneous coronary intervention), may be lifesaving, but reperfusion might exacerbate the cellular damage, and changes in the endothelium are believed to be involved in this worsened outcome.AimThe aim of the present study was to compare endothelial dependent and independent vasodilatory effect after experimental myocardial ischemia/reperfusion (I/R).MethodsA well-established rat model of myocardial ischemia with 24 h of reperfusion was applied, followed by a study in a wire myograph.ResultsEndothelial NO dependent relaxation in response to carbachol, was sensitive to arterial depolarization, and was unaffected by I/R. In contrast, endothelial NO dependent ADPβS signalling, which was not sensitive to arterial depolarization, was significantly reduced after I/R. Following I/R, an H2O2 dependent EDH induced dilation appears in response to both of the above agonists. In addition, calcitonin gene-related peptide (CGRP) induced vasodilation was reduced.ConclusionThese data show that NO dependent ADPβS induced dilation is reduced after I/R. However, there is some compensation by released H2O2 causing an EDH. Combined with a loss of maximal dilation in response to CGRP, the reduced vasodilation could be an important factor in understanding the exacerbated damage after I/R.