BackgroundNitric oxide (NO) is protective for the cardiovascular system, and excessive NO exerts negative effects on the circulatory system. This study aimed to compare the effects of selective or non-selective NO synthase (NOS) inhibitors on blood flow perfusion of ischemia-reperfused myocardium.Materials/MethodsMale mongrel dogs were randomly assigned to 4 groups: only ischemia-reperfusion (control), ischemia-reperfusion plus Nω-nitro-L-arginine methyl ester (NAME) treatment, ischemia-reperfusion plus aminoguanidine (AMD) treatment, and sham operation group. Myocardial contrast echocardiography (MCE) was performed. Blood samples were taken for measurement of NO. Background-subtracted peak videointensity (PVI) and PVI ratio in myocardium were measured.ResultsIn the NAME-treated group, the PVI at 5 min reperfusion did not significantly differ from pre-LAD-occlusion, but declined to and retained at a level obviously lower than the pre-LAD-occlusion. In the AMD-treated group, the PVI at 5 min reperfusion was significantly higher than at pre-LAD-occlusion, and then restored to and remained at the pre-LAD-occlusion level. The changes of PVI ratios in the 3 groups were similar to PVI values. In the AMD-treated group, the curve width increased in the early reperfusion, but returned to the pre-LAD-occlusion level at 90 min reperfusion. The plasma NO concentration in the NAME-treated group greatly decreased and remained low during the whole period of reperfusion. In the AMD-treated group, there were only slight increases in NO concentrations during reperfusion.ConclusionsNAME totally inhibited NO production and attenuated myocardial blood flow perfusion. Aminoguanidine significantly relieved the increase in NO production and alleviated the congestion of reperfused myocardium. Selective inhibitors of iNOS might be useful in the management of certain diseases associated with ischemia-reperfusion.

Objective: To investigate changes in the coronary microcirculation during myocardial stunning in dogs. Methods: Male mongrel dogs underwent a 15- or 60-min occlusion of the left anterior descending coronary artery, followed by a 120-min reperfusion. Myocardial contrast echocardiography was performed before and after treatment with acetylcholine (ACH) or nitroglycerin (NG). Peak videointensity (PVI) in the myocardial zone was measured, and myocardial samples were examined using transmission electron microscopy. Results: In the 15-min group, the ratio of the PVI between the stunned and intact myocardial zone (PVIR) before and after treatment with NG (NG-PVIR) or ACH (ACH-PVIR) declined markedly in the early period of reperfusion and then returned to preligation levels. In the 60-min group, NG-PVIR was reduced in the early period of reperfusion and then returned to its preligation level. A low level of ACH-PVIR lasted during the entire 120-min reperfusion. Similar changes in the ratio of the PVIR before and after treatment with NG or ACH were observed. In the 60-min group, capillary endothelial edema and widening of intercellular linking gaps were observed. Conclusions: We observed microvascular endothelial damage and endothelium-dependent dilatation impairments in stunned myocardium, and their severity and recovery rate are affected by the duration of ischemia.