Effects Of Sodium Ferulate On No-reflow In Rats Of Acute Myocardial Infarction And Reperfusion

ObjectiveInvestigate of sodium ferulate on the no-reflow phenomenon in rats aftermyocardial ischemia reperfusion, as well as the possible mechanisms toimprove no reflow.MethodsFifty-six healthy male Wistar rats were randomly and equivalently dividedinto4groups：(1).sham group(2).control group(3).sodium ferulategroup(4)sodium ferulate plus L-NNA group. Sodium ferulate20mg/Kg was givento rats30min before ischemia. before reperfusion15min, the nitric oxidesynthase blocker L-NNA，15mg L/kg by tail vein injection.To generate the animalmodel mimicking the no-reflow phenomenon, the rats first received occlusion ofthe Left anterior descending artery for60min and then followed120min ofreperfusion. After120min of reperfusion, blood serum CK-MB content,Thioflavin S, Evans blue living tissue staining, observed in the rat of myocardialno reflow and ischemia area; Triphenyl tetrazolium chloride staining assess ratmyocardial infarction area; The myocardial tissue detect the NO content;Immunohistochemical method to detect iNOS and eNOS protein content inmyocardium and heart blood vessels; Microvascular endothelial and observedunder electron microscope mitochondria damage.ResultsTo the control group, AMI/R group serum CK-MB was obviously increased(5031.50±353.38:1187.75±204.59, P<0.01), eNOS protein reduced (0.18±0.04:0.25±0.05,0.30±0.04:0.46±0.10, P<0.05)), iNOS protein increased (0.39±0.01: 0.22±0.02,0.59±0.05:0.26±0.02, P<0.01), myocardial NO content reduce(17.29±3.55:49.52±1.97, P<0.01), under electron microscopy microvascularendothelial damage obviously, myocardial mitochondria severe swelling,membrane and crest fracture, no-reflow scope and range of infarction area islarger, ischemic range is no obvious change. compared withischemia-reperfusion group, Sodium ferulate group, serum CK-MB(2695.50±379.91:5031.50±353.38, P<0.01), eNOS protein increase (0.30±0.03:0.18±0.04,0.62±0.06:0.476±0.10, P<0.01), iNOS protein reduced (0.32±0.02:0.39±0.01,0.43±0.04:0.59±0.05, P<0.01), and myocardial content of NOincreased (35.46±3.67:17.29±3.55, P<0.01),under electron microscopy,microvascular endothelial damage reduce, myocardial mitochondrial swellingin mild-to-moderate, myocardial infarction range (86.40±7.45:66.78±7.49,P<0.05), the range of myocardial no-reflow reduce(50.53±6.77:33.08±6.87,P<0.01),the scope of ischemia did not see obvious difference.Compared with Sodium ferulate group, ferulic acid sodium serum+L-NNAgroup, CK-MB was significantly higher(3790.25±367.61:2695.50±379.91,P<0.01), the eNOS and iNOS content showed no statistical difference (P>0.05),increase scope of myocardial no-reflow(50.53±6.77:47.19±8.52, P>0.05),infarction range increased(86.40±7.45:76.20±8.17, P<0.05), myocardial tissueNO decreased production(17.29±3.55:20.00±2.75, P>0.05).ConclusionsSodium ferulate can significantly reduce the myocardial ischemiareperfusion in rats and infarction area of no-reflow area, its mechanism may bethrough regulate NOS-NO way, inhibition of iNOS protein expression ofmyocardial and vascular, promote eNOS protein expression, increase the NOlevel in the organization. However, NOS blockers L-NNA can block theprotection reflow of the sodium ferulate in rats with myocardial ischemiareperfusion, suggesting that NO may be playing an important role in theprevention and controling of NO reflow.