| Objective: To observe the influence of hyperhomocysteinemia onno-reflow after acute myocardial infarction reperfusion in rats, evaluate the roleof captopril on no-refiow after acute myocardial infarction reperfusion inhyperhomocysteinemia rats,and investigate its mechanism.Methods: Forty SD rats were randomly divided into the normal blankgroup (10),the normal control group (10),the Hhcy-model group(10),and thecaptopril intervention group (10), the female and male were divided equally.During the period of breeding,the normal blank group were administered withnormal diet,the normal control group were intraperitoneal injected withphysiological saline5ml/Kg and filled the stomach by given saline5ml/Kgonce daily,the Hhcy-model group were intraperitoneal injectedwith2%L-cysteine5ml/Kg and filled the stomach by given saline in equalvolumes of the above.the captopril intervention group were intraperitonealinjected with2%L-cysteine5ml/Kg,and filled the stomach by given captopril8.75mg/Kg,all the rats were feeding in animal feed and water.this procedurecontinuously for12weeks, At the end of the twelfth weeks,all the rats wereintraperitoneal injected with Soluble Pentobarbitone(45mg/Kg) to anesthesiathem,the tracheal intubation were given and connected the rats with smallanimal respirator to assist their breathing ((set respiratory frequency80times/min, tidal volume of19.6mL/Kg)), and monitoring their ECG.thenexposed the heart and ligated the anterior descending branch for90min(thenormal blank group thread only without ligation),then cut the ligature andreperfusion for90min,sacrifice the rats and take arterial blood to separatingplasma,and detected the level of Hcy, LDH, TN-I, MDA, CATand P-S. Then,take5rats randomly to the Evan’s blue myocardial staining.At last, take5rats of the rest to the HE myocardial staining.Results:①t he level of Hcy:the level of Hcy in the Hhcy-model group andcaptopril intervention group were significantly higher than that of normal blankgroup and normal control group (P <0.001).②The changes of ECG:There wasno significant alteration in the ECG of the normal blank group,the othergroup’s p-p interval in the ECG was extended than normal after deligation theLAD for90mintues.(normal blank group p<0.05,the Hhcy-model group andcaptopril intervention group p<0.01),Elevated ST-segment and T-wave fused asa single curve(p<0.01).Compared with reperfusion for90min after loosen theligature and the coronary artery ligation period,the ST-segment of Captoprilintervention group regression significantly (P <0.05),but those had nosignificant changes in the Hhcy-model group and the normal controlgroup.③t he levels of the plasma LDH,TN-I in the Hhcy-model group weresignificantly increased than the normal control group (P<0.001),while those inthe captopril intervention group were significantly decreased(P<0.001).④theactivity of plasma CAT of the Hcy-modle group were significantly decreasedthan the normal control group（P＜0.001),while those were significantlyincreased in the captopril intervention group（P＜0.001). The level of plasmaMDA of the Hcy-modle group were significantly increased than the normalcontrol group（P＜0.001),while those were significantly decreased in thecaptopril intervention group （P＜0.001).⑤In the Hhcy-model group,theexpression of the plasma P-S were ignificantly increased than the the normalcontrol group （P＜0.001）,on the contrary,the captopril intervention groupwere significantly decreased than the Hhcy-model group（P＜0.001）.⑥Therange of no-reflow after Evan’s blue staining:the no-reflow range of the fiverats in the normal blank group is15.15%.the no-reflow range of the five rats in the Hhcy-model group is27.27%.And the captopril intervention group is13.73%.⑦The myocardial HE dyeing:the myocardial cells of the normal blankgroup were completely and the nucleus shape was normal,the muscle fiberswere arranged neatly.But in the normal control group,there were visible focalnecrosis on the myocardial cells, dissolved muscle fibers,and the myocardialinterstitial edema, inflammatory cells infiltrated around them.Above changeswere more grave in the Hhcy-model group but were alleviative in the captoprilintervention group.Conclusion: The activity of plasma CAT were significantly decreased, but thelevel of plasma MDA,P-S were significantly increased after acute myocardialinfarction reperfusion, illustrate oxidative stress and inflammatory reactionwere reinforced in reperfusion period. Further confirmed that the oxidativestress and inflammatory reaction were one of the important reasons of AMIno-reflow after reperfusion. The activity of plasma CAT were further decreased,but the level of plasma MDA, P-S were further increased, illustrate Hhcy is theimportant reason of no reflow.The possible mechanism is associated withoxidative stress, inflammatory reaction. By myocardial Evan’s blue staining ofreperfusion animal detect there was no reflow after reperfusion, Hhcy canincrease the no reflow area. Captopril can’t reduce plasma hcy concentration,But can effectively reduce Hhcy AMI no reflow after reperfusion in rats byreducing oxidative stress and inflammatory reaction mechanism. Characterizedby captopril can make plasma activities of CAT, MDA and P-S contentdecreased. |
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