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Objective To explore the ischemic myocardial perfusion and viability.Methods Ten successful pigs with myocardial infarction model underwent MRI first-pass myocardial perfusion examinations preoperatively and 24 hours,72 hours and one week postoperation.After MRI examinations,the experimental pigs were executed and the samples underwent TTC staining and pathological examination.Results The preoperative myocardial perfusion in the all of the 10 pigs was nomal,but there were myocardial perfusion decrease and defects in 8 experimental pigs after operation,the perfusion curves in the area with perfusion defects had no obvious peak,but there was gradual increase in the end of the performance.The perfusion peak of the area with perfusion decrease was lower than that of normal inferior and lateral myocardial wall(P＜0.05) and the peak perfusion time was delayed compared with that of normal inferior and lateral myocardial wall (P＜0.05).There was myocardial necrosis in the perfusion defects areas that was certified by TTC staining and pathological examination.The intersititial edema and myocardial degeneration could be seen in the perfusion reduced areas.Conclusion MRI fist-pass myocardial perfusion imaging combined with perfusion curve analysis can evaluate the perfusion changes of the regional myocardial microcirculation.
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[Objective] To observe the effect of HQSM on PGI_2/TXA_2 in blood plasma of acute myocardial ischemia rats caused by injecting pituitrin. [Methods] 84 SD rats were divided into seven groups at random: normal control group,model control group,three HQSM groups(210mg/kg,150mg/kg,105mg/kg),Huangqi Shengmaiyin and DI’ao Xinxuekang. Intragastric administration was adopted once a day for 30 days.Acute myocardial ischemia model rat was established by injecting pituitrin from tail vein 1h after the last administration, and blood plasma was separated to be determined the activity of 6-Keto-PGF_ 1? and TXB_2, which is the metabolite of PGI_2 and TXA_2 in blood plasma of SD rats. [Results] Having been injected pituitrin,the activity of TXB2 upgraded while 6-Keto-PGF_ 1? /TXB_2 decreased(P
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Recently, autologous bone marrow cell transplantation (CTx) for angiogenesis and myogenesis in ischemic myocardium has been extensively investigated to improve heart function. This study was designed to evaluate the effects of CTx with off-pump coronary artery bypass grafting (OPCAB) in patients who were not feasible for complete revascularization. Seven male patients underwent CTx combined with OPCAB in 5, CTx only in 1, and mitral valve repair in 1 patient simultaneously. Bone marrow was aspirated from iliac bone. Mean 1.5 x109 mononuclear cells including mean 7.3 x106 CD34+ cells and 2.4 x106 AC133+ cells were obtained and concentrated with 10cc. These cells were transplanted into non-graftable ischemic myocardium. Heart function was evaluated in all patients using MIBI scan, echocardiogram and heart magnetic resonance imaging (MRI) preoperatively. The effect of CTx was evaluated using MIBI scan, echocardiogram, and MRI postoperatively. An average of 2 grafts were bypassed. Other territories were transplanted with isolated mononuclear cell. All patients had an uncomplicated postoperative course. After 2 to 7 months follow-up, there was improvement in symptom, ejection fraction (from 43% to 47%) on echocardiogram and myocardial perfusion on MIBI scan and MRI in all patients. These preliminary data showed improvement of heart function and myocardial perfusion and also showed the feasibility and safety of combined therapy with OPCAB and CTx in ischemic myocardium. However, the effectiveness of CTx alone cannot be readily assessed. Further randomized, controlled studies are required to evaluate the effectiveness of CTx alone.
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Objective:To study the effect of Levocarnitine preconditionon on the myocardial ultrastructure of ischemic rats and the long last calcium channel. Methods: We randomly divided 30 rats into a control group, a Levocarnitine group and a Dihydrochloride group. After the establishment of ischemic models, we observed the ultrastructure of the ischemic myocardium with optical and transmission electron microscopes, and detected the influx of calcium in the long last calcium channel with the patch clamp. Results: Levocarnitine protected the ultrastructure of ischemic myocardium and inhibited the influx of calcium in the long last calcium channel. Conclusion: Levocarnitine can reduce the severity and extent of ischemia-induced damage to the myocardium, protect mitochondria, stabilize its oxidation, inhibit the long last calcium channel of ischemic ventricular myocytes and lessen the injury induced by calcium overload.
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Objective To investigate the feasibility in improving the heart function by smooth muscle cells transplantation into the ischemic myocardium model established by coronary artery ligation. Methods Myocardial infarct was produced by ligation of the left coronary artery. At 2 weeks after establishment of myocardial infarct, cultured fetal rat gatric smooth muscle cells marked with BrdU were transplanted into the ischemic myocardium by direct injection (transplantation group, n=10), or culture medium alone (control group, n=10). Heart function was assessed by echocardiography before and at 4 weeks after transplantation. At 4 weeks after transplantation, the hearts were harvested. The transplanted smooth muscle cells were assessed by immunostaining against BrdU and ?-SMA. Results The injected fetal smooth muscle cells survived in the infarcted regions and formed muscle-like tissues at the site of transplantation at 4 weeks after transplantation. The grafts thickened the wall of the left ventricle [(2.51?0.22) mm vs (1.32?0.16) mm, P