Effect of Rosuvastatin on Myocardial Inflammation and Left Ventricular Disfunction After Coronary Microembolization in Rats 瑞舒伐他汀对大鼠冠状动脉微栓塞后心肌局部炎症反应及左心室功能的影响
Effects of fenofibrate on myocardial inflammation and ventricular remodeling of diabetic cardiomyopathy rats 非诺贝特对糖尿病性心肌病大鼠心肌炎症和心室重塑的影响
Effects of experimental acute myocardial infarction ( AMI) on rabbits with systemic inflammation 急性炎症状态对家兔急性心肌缺血的影响
Conclusions Plasma N-BNP correlates with the state of myocardial microcirculatory reperfusion and inflammation. 结论AMI再灌注过程中血浆N-BNP与炎性细胞因子水平同步增高,其增高水平与心肌组织灌注状态密切相关。
Conclusion Immunological activation and myocardial inflammation exist in CHF patients. 结论CHF患者存在免疫激活和心肌炎症反应,心衰程度越重,炎症反应也越明显。
The ischemia preconditioning of cardiac muscle group and needle prick preconditioning group is iower than myocardial ischemia group in the damage of cardiac muscle fiber edema extent and inflammation cellular infiltration. 与心肌缺血组相比,心肌缺血预处理组、针刺预处理组心肌纤维破坏不明显,水肿程度轻,炎细胞浸润较少。
Viral myocarditis ( VM) is the viral infection desease, which is characterized by myocardial inflammation. 病毒性心肌炎(ViralMyocarditis,VM)是由亲心肌病毒感染所致的以心肌炎症病变为主的疾病。
Viral myocarditis refers to human infections thermophilic centricity virus that causes the myocardial nonspecific interstitial inflammation. 病毒性心肌炎是指人体感染了嗜心性病毒,引起的心肌非特异间质性炎症。
In myocardial infarction, they actively participate in postinfarction inflammation, while also regulating fibrous tissue deposition and angiogenesis during the proliferative phase of healing. 在心肌梗塞中,肥大细胞调节了梗塞后的炎症反应以及愈合期的心肌纤维的沉积和血管的形成。
The mechanism of cardiovascular and cerebrovascular disease was caused by free radicals which processed by myocardial ischemia and reperfusion, inflammation, etc. The free radicals could damage of biological macromolecules 、 lead to lipid peroxidation and protein cross-linking. 许多心脑血管疾病发生机制是心肌缺血再灌注、炎症反应等过程产生的自由基损伤生物大分子,导致脂质过氧化、蛋白质交联等变化,而抑制自由基反应,是缓解此类损伤的重要途径。
The main pathological changes of DCM are microvascular endothelial cells impairment, collagen fibers in endocardium proliferation, vascular basement membrane thickening, myocardial interstitial inflammation and fibrosis as well as cardiomyocytes hypertrophy and apoptosis. 糖尿病心肌病的主要病理改变是心肌微血管内皮细胞损害,内膜下纤维增生,血管基底膜增厚,心肌间质炎症和纤维化,心肌细胞肥大、凋亡。
It has been reported that the size of myocardial necrosis, the damage extent of myocardial function are high associated with the level of various inflammatory factors. The critical role of inflammation regulation factors and inflammatory responses in ischemia-reperfusion injury becomes more and more being recognized. 有研究表明缺血性心脏病人心肌细胞坏死情况和心脏功能损伤程度的大小及炎症因子水平的多少密切相关,可见各种炎症调节因子以及炎症反应在心肌缺血再灌注损伤中起着越来越重要的作用。
Myocardiac fibrosis can be caused by myocardial ischemia, overload, hypoxia, inflammation, which occurs in different cardiovascular diseases. 在许多心血管疾病发生时,由于心肌负荷过重、缺血、缺氧和炎症等原因常常会引起心肌纤维化的形成。
Clarify tanshinone IIA injection on myocardial ischemia-reperfusion injury mechanism is inhibition of inflammation. 4. 阐明丹参酮IIA磺酸钠注射液对心肌缺血-再灌注损伤保护机制主要是抑制炎症反应。
CMR delayed enhancement examination could dynamically observe the changes of myocardial inflammation, it can be used in the follow-up of VMC. 磁共振心肌延迟增强扫描可以动态观察心肌炎症的变化,可用于病情随访。