Infarcted Area Of Heart Research Articles

Effects of nalbuphine on the cardioprotective effect of morphine in rats

BackgroundWhen combined with morphine, nalbuphine not only does not affect the analgesic effect but also prevents opioid-induced side effects. The authors investigated whether nalbuphine interferes with morphine-induced cardioprotection in rats. MethodsAnesthetized male Sprague-Dawley rats were randomly assigned to 1 of 4 treatment groups. Nalbuphine (NAL, 1 mg/kg) and morphine (MOR, 0.3 mg/kg) were administered 10 and 5 min prior to myocardial ischemia, respectively. Additionally, the NAL + MOR group received the combination of NAL and MOR prior to myocardial ischemia. An in vivo animal model was established by occluding the left anterior descending artery for 30 min and reperfusing it for 2 h. After 2 h of reperfusion, the infarcted area of heart was measured by Evans blue/triphenyl tetrazolium staining, and the levels of creatine kinase isoenzymes (CK-MB) in serum were detected by enzyme-linked immunosorbent assay. ResultsNalbuphine had no protective effect against the infarct area compared with the control treatment (NAL, 52.5 ± 5% versus CON, 52.6 ± 4%; *P < 0.01), and the infarct size-sparing effects of morphine were not affected by nalbuphine (NAL + MOR, 42.6 ± 7% versus MOR, 40.4 ± 3%; P > 0.05). The nalbuphine group did not show a change the levels of serum CK-MB compared with the control group, and nalbuphine did not affect the levels of serum CK-MB in the MOR group. ConclusionsNalbuphine does not interfere with the cardioprotective effect of morphine in vivo. Therefore, nalbuphine could be safely used or combined with morphine in patients with acute myocardial infarction.

Effect of human thymus adipose tissue-derived mesenchymal stem cells on myocardial infarction in rat model

Background and objectiveStem cell (SC) therapy exhibits promising therapeutic efficiency against cardiovascular disease. The thymus adipose tissue (TAT) is familiar to cardiac surgeons with sternotomy; however, the application of TAT in SC therapy remains unknown. We assessed the effectiveness of TAT-derived mesenchymal SCs (TAT-MSCs) in the rat myocardial infarction (MI) model.MethodsThe human TATs were obtained from the patients who underwent coronary artery bypass graft surgery. In cell studies, we performed the cumulative population doubling level assessment, fluorescence-activated cell sorting analysis, and differentiation study. In animal studies, we segregated Sprague–Dawley rats (ischemia-reperfusion model) into three (sham, vehicle, and TAT-MSC) groups based on their corresponding treatment. Trans-thoracic echocardiogram (TTE) was obtained to assess the recovery of heart function in the 1st, 4th, 8th, and 12th week after surgical manipulations. After echocardiographic study, infarcted area of the heart was measured using triphenyl tetrazolium chloride (TTC) stain.ResultsThe sham group exhibited significantly better systolic and diastolic function (SDF) than the other groups did. After one week of TAT-MSC or vehicle injection, the TAT-MSC group exhibited a significant improvement in the E/E′ value (25.75 ± 1.09 vs. 24.20 ± 0.91, p < 0.001) compared to the vehicle group. Although statistically insignificant, the trend of improvement in SDF was better in the TAT-MSC group than in the vehicle group. The infarcted area measured by TTC staining was 22.81 ± 6.41% and 29.95 ± 9.09% in the TAT-MSC and vehicle groups, respectively (p = 0.04).ConclusionAlthough TTE results exhibited insignificant variations in SDF, a trend with improvement in the SDF of the heart was observed in the TAT-MSC group compared to the vehicle group. The infarcted area of heart indicated significant reduction in the TAT-MSC group compared to the vehicle group as confirmed by histopathological study.

Study on the therapeutic effects of hyperbaric oxygen on human umbilical cord Wharton jelly mesenchyme cells on myocardial infarction rats

Objective To explore whether hyperbaric oxygen could enhance the effects of the transplanted stem cell on treating myocardial infarction rats. Methods A total of 70 Sprague-Dawley (SD) Rats was randomly divided into four groups, sham operated, acute myocardial infarction (AMI), mesenchymal stem cells (MSCs) (Stem Cell Transplanting), and hyperbaric oxygen (HBO) + MSCs group, respectively. Myocardial infarction rat model was established, hyperbaric oxygen treatment was carried out every day at the first to 30 day after AMI. Human umbilical cord Wharton jelly mesenchyme cell was transplanted at the third day after AMI. The densities of polymorphonuclear neutrophils and macrophages in the infracted border zones and in the infarcted area of heart were determined with hematoxylin and eosin (HE) staining. The cardiac function was assessed with M-mode transthoracic echocardiography, in vivo. Results ⑴Compared to MSCs group, the stem cell proliferation and survival rates were increased significantly at the forth week (276.6±73.8 versus 20.5±12.3, P 0.05). Conclusions Hyperbaric oxygenation could significantly promote the proliferation and survival rate of stem cells, and improve the cardiac function. Thus further enhance the effect of the transplanted stem cell on treating the in-farcted heart. Key words: Hyperbaric oxygenation; Mesenchymal stem cell transplantation; Myocardial infarction/SU; Umbilical cord/CY/SU

Abstract 372: Regulation of Ski and Scleraxis in the Infarcted Rat Heart

Introduction: Coronary heart disease is causal to myocardial infarction (MI) and cardiac fibrosis. Upon ischemic myocardial injury, resident cardiac fibroblasts phenoconvert to myofibroblasts and synthesize large amounts of fibrillar collagens to produce scar tissue. Although the myofibroblast numbers are reduced in the infarct scar following the completion of wound healing, a sub-population of cells persist in the wounded area, leading to maladaptive chronic remodeling of the scar area and eventually the non-infarcted myocardium. Ski has been identified as a repressor of the TGF-β1 signaling pathway, attenuating the myofibroblast phenotype and its functional properties. Scleraxis has been implicated in canonical TGF-β1 signaling to promote collagen1α2 expression. We investigated how Ski and Scleraxis contribute to physiological and pathological wound healing in vivo. Methods: The study was carried out using 64 male Sprague-Dawley rats. The left anterior descending (LAD) coronary artery was ligated to induce a myocardial infarction. Control (sham) operated animals underwent surgery without ligation of the LAD artery. Animals were sacrificed at 2, 4, and 8 weeks post-MI and tissue collected for Western blot and qPCR studies. Results: Scleraxis mRNA expression remained at baseline at 2 and 8 weeks post-MI, but was significantly increased 4 weeks post-MI. Scleraxis protein expression was down-regulated within the scar area of infarcted hearts when compared to control samples 2 and 4 weeks post-MI. Ski mRNA expression was up-regulated within the scar area of infarcted hearts 2, 4 and 8 weeks after infarction. Conclusions: Scleraxis protein is down-regulated in myofibroblasts of the infarct scar in the chronic stages of myocardial infarction, corresponding to the maturation of the scar. At these stages of wound healing, we have previously published that Ski is up-regulated in the cytosol of these same cells. We suggest reciprocal feedback in the expression of these two proteins exists in myofibroblasts in the infarct scar. We hope to learn more about the Ski/Scleraxis feedback loop in pathological wound healing to identify novel therapeutic targets.