• Journal of Chest Surgery
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• v.54 no.1
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• pp.9-16
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• 2021

Background: The deposition of monomeric C-reactive protein (mCRP) in the myocardium aggravates ischemia-reperfusion injury (IRI) and myocardial infarction. Ischemic preconditioning (IPC) is known to protect the myocardium against IRI. Methods: We evaluated the effects of IPC on myocardium upon which mCRP had been deposited due to IRI in a rat model. Myocardial IRI was induced via ligation of the coronary artery. Direct IPC was applied prior to IRI using multiple short direct occlusions of the coronary artery. CRP was infused intravenously after IRI. The study included sham (n=3), IRI-only (n=5), IRI+CRP (n=9), and IPC+IRI+CRP (n=6) groups. The infarcted area and the area at risk were assessed using Evans blue and 2,3,5-triphenyltetrazolium staining. Additionally, mCRP immunostaining and interleukin-6 (IL-6) mRNA reverse transcription-polymerase chain reaction were performed. Results: In the IRI+CRP group, the infarcted area and the area of mCRP deposition were greater, and the level of IL-6 mRNA expression was higher, than in the IRI-only group. However, in the IPC+IRI+CRP group relative to the IRI+CRP group, the relative areas of infarction (20% vs. 34%, respectively; p=0.079) and mCRP myocardial deposition (21% vs. 44%, respectively; p=0.026) were lower and IL-6 mRNA expression was higher (fold change: 407 vs. 326, respectively; p=0.376), although the difference in IL-6 mRNA expression was not statistically significant. Conclusion: IPC was associated with significantly decreased deposition of mCRP and with increased expression of IL-6 in myocardium damaged by IRI. The net cardioprotective effect of decreased mCRP deposition and increased IL-6 levels should be clarified in a further study.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.1
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• pp.17-21
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• 2018

Our previous studies have confirmed that morroniside has neuroprotective effects. However, the effects of morroniside on cardiac myocardium remain unknown. Rats were anaesthetized with 10% chloral hydrate (0.35~0.4 mL/kg) and an acute myocardial infarction (AMI) was induced by ligating the anterior descending coronary artery (LAD). Following AMI, morroniside was administered intragastrically for 3 consecutive days at doses of 45, 90 and 180 mg/kg, respectively. Lactate dehydrogenase (LDH) and cardiac troponin T (cTnT) activities in AMI rats in the serum were detected with commercial kits. The expression of IL-6, $IL-1{\beta}$ and $TNF-{\alpha}$ in myocardium was detected by Western blotting analysis. We observed a significant decline in the Q(q) wave amplitude in morroniside-treated rats after 72 h. Additionally, treatment of morroniside decreased the levels of LDH and cTnT in AMI rats. We also observed that morroniside reduced the expression of IL-6, $IL-1{\beta}$ and $TNF-{\alpha}$ in myocardium. Taken together, our findings demonstrate that morroniside had effective anti-inflammatory properties in AMI rats.

• Proceedings of the KSMRM Conference
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• 2003.10a
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• pp.43-43
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• 2003

Viable myocardium can be distinguished from the infarcted myocardium by contrast-enhanced magnetic resonance imaging (ceMRI). In this study, contrast-enhancement with cine magnetic resonance imaging (cecineMRI) was performed for direct correlation of transmural extent of hyperenhancement and that of contractility.

• Proceedings of the KSMRM Conference
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• 2003.10a
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• pp.89-90
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• 2003

Viable myocardium can be distinguished from the infarcted myocardium by contrast-enhanced magnetic resonance imaging (ceMRI). In this study, contrast-enhancement with cine magnetic resonance imaging (cecineMRI) was performed for direct correlation of transmural extent of hyperenhancement and that of contractility.

• 한국생물공학회:학술대회논문집
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• 2003.04a
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• pp.95-97
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• 2003

Despite recent advances in the treatment of acute myocardial infarction, the ability to repair extensive myocardial damage is limited. To develop a new therapy for myocardial infarction, we examined the possibility of regenerating myocardium by implanting bone marrow-derived mononuclear cells(BM-MNC) . Histological and immunohistochemical examination showed myocardium regeneration and angiogenesis in the cell transplantation site. Isolated perfused (Langendorff) heart experiments revealed enhanced functions of heart. These results suggest that BM-MNC transplantation induce cardiac muscle regeneration and that this approach could be applied as a possible treatment for myocardial infarction.

• 한국생물공학회:학술대회논문집
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• 2003.10a
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• pp.164-166
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• 2003

Despite recent advances in the treatment of acute myocardial infarction, the ability to repair extensive myocardial damage is limited. Revascularization in ischemic myocardium is required to improve cardiac function and prevent further scar tissue formation. Bone marrow contains endothelial precursors that can be used to induce neovascularization in ischemic myocardium. To develop a new therapy for myocardial infarction, we investigated if implantation of bone marrow mononuclear cells (BM-MNCs) using biodegradable matrices could enhance neovascularization in ischemic myocardium. Eight weeks after implantation, the damaged myocardium implanted with BM-MNCs and fibrin gels exhibited significantly greater angiogenic responses than those implanted with either fibrin gels or BM-MNCs alone. Fibrin gels disappeared completely 8 weeks after implantation. Echocardiography revealed improved heart functions. These results suggest that implantation of BM-MNCs using fibrin gel matrix efficiently induces neovascularization and improved heart functions in ischemic myocardium.

• Korean Journal of Radiology
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• v.2 no.1
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• pp.21-27
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• 2001

Objective: To identify and evaluate the lateral border zone by comparing the size and distribution of the abnormal signal area demonstrated by MR imaging with the infarct area revealed by pathological examination in a reperfused myocardial infarction cat model. Materials and Methods: In eight cats, the left anterior descending coronary artery was occluded for 90 minutes, and this was followed by 90 minutes of reperfusion. ECG-triggered breath-hold turbo spin-echo T2-weighted MR images were initially obtained along the short axis of the heart before the administration of contrast media. After the injection of Gadomer-17 and Gadophrin-2, contrast-enhanced T1-weighted MR images were obtained for three hours. The size of the abnormal signal area seen on each image was compared with that of the infarct area after TTC staining. To assess ultrastructural changes in the myocardium at the infarct area, lateral border zone and normal myocardium, electron microscopic examination was performed. Results: The high signal area seen on T2-weighted images and the enhanced area seen on Gadomer-17-enhanced T1WI were larger than the enhanced area on Gadophrin-2-enhanced T1WI and the infarct area revealed by TTC staining; the difference was expressed as a percentage of the size of the total left ventricle mass (T2= 39.2 %; Gadomer-17 =37.25 % vs Gadophrin-2 = 29.6 %; TTC staining = 28.2 %; p < 0.05). The ultrastructural changes seen at the lateral border zone were compatible with reversible myocardial damage. Conclusion: In a reperfused myocardial infarction cat model, the presence and size of the lateral border zone can be determined by means of Gadomer-17- and Gadophrin-2-enhanced MR imaging.

• International Journal of Stem Cells
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• v.17 no.1
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• pp.70-79
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• 2024

The efficacy of adipose-derived stem cells (ASCs) on myocardial infarction is limited due to poor survival and engraftment. Integrin-mediated cell adhesion is a prerequisite for its survival and homing. ASCs expressed insufficient integrin 𝛼₄, limiting their homing capacity. This study aims to characterize integrin 𝛼₄⁺ ASC subpopulation and investigate their therapeutic efficacy in myocardial infarction. We used fluorescence-activated cell sorting to harvest integrin 𝛼₄⁺ ASCs subpopulation, which were characterized in vitro and transplanted into myocardial infarction model. Positron emission tomography imaging were performed to measure infarction size. Cardiac cine magnetic resonance imaging was used to evaluate heart contractile function. Compared with the unfractionated ASCs, integrin 𝛼₄⁺ ASCs subpopulation secreted a higher level of angiogenic growth factors, migrated more rapidly, and exhibited a stronger anti-apoptotic capacity. Vascular cell adhesion molecule-1 was obviously up-regulated at 3 days after myocardial infarction, which interacted with integrin α₄ receptor on the surface of ASCs to enhance the survival and adhesion. Thus, we implanted unfractionated ASCs or integrin α₄⁺ ASCs subpopulation into the 3-day infarcted myocardium. Integrin α₄⁺ ASCs subpopulation exhibited more robust engraftment into the infarcted myocardium. Integrin α₄⁺ ASCs subpopulation more effectively decreased infarct size and strengthen cardiac function recovery than did the unfractionated ASCs. Integrin α₄⁺ ASCs subpopulation is superior to unfractionated ASCs in ameliorating ischemic myocardial damage in animal model. Mechanistically, their more robust engraftment into the infarct area, higher migratory capacity and their increased release of paracrine factors contribute to enhanced tissue repair.

• Nuclear Medicine and Molecular Imaging
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• v.42 no.6
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• pp.478-481
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• 2008

Reverse redistribution is frequently observed after revascularization in acute myocardial infarction, and usually regarded as a predictor of viable myocardium on stress/rest and 2- to 4-hour redistribution $^{201}Tl$ SPECT. However, there is not enough report of reverse redistribution in case of 24-hour delayed SPECT, which is commonly used for viability assessment. In this report, a case of reverse redistribution on rest and 24-hour delayed $^{201}Tl$ SPECT is reported with use of automatic segmental quantitative analysis. The myocardium of reverse redistribution was dysfunctional on gated SPECT, and diagnosed as non-viable on $^{18}F-FDG$ PET.

• Investigative Magnetic Resonance Imaging
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• v.7 no.2
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• pp.132-136
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• 2003

Purpose : To evaluate the usefulness of breath-hold T2-weighted MR imaging in patients with myocardial infarction. Materials and Methods : We investigated 11 patients with myocardial infarction who shown delayed enhancement on MR imaging. Infarcted myocardium on T2-weighted MR imaging was classified as high, iso, and low signal area comparing with normal myocardium. The intensity and transmural extent of infracted myocardium was also analyzed. On the basis of clinical information, the stage of infracted myocardium on T2-weighted MR imaging was assessed. Results : It was observed high signal area in 12 segments of 5 patients, low in 12 segments of 6 patients on T2-weighted MR imaging. The high signal intensity of infarcted myocardium was shown as $175{\pm}9\%$ comparing with that of the normal myocardium, low signal intensity as $73{\pm}5\%\;(p\;<\;0.05)$. In the evaluation of transmural extent, the high signal areas on T2-weighted MR imaging were larger than infarct area on delayed enhancement imaging $(100\%\;vs.49\%{\pm}17\%)$, whereas low signal areas on T2-weighted MR imaging correlated. High signal area was visualized on T2-weighted MR imaging within 11 days, whereas low-signal area was seen after 7 months. Conclusion : Breath-hold T2-weighted MR imaging is useful in the evaluation of stage as well as edema and fibrous scar in patients with myocardial infarction.