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冠心病的发病机制涉及到肥大细胞,在IgE介导下肥大细胞可释放多种血管活性物质影响局部血流。临床资料用酶免疫法对100例急性心肌梗塞(AMI)患者和16名无AMI证据的急性冠脉供血不足(acute coronary insufficiency, ACI)者作了连续血清IgE浓度测定和血嗜酸性细胞计数。结果AMI后平均血清IgE浓度逐渐增高,第7天达峰值,14天后下降,第3周末降至接近正常水平。有少数病人持续不降。IgE增高的同时血嗜酸细胞计数增加。ACI组IgE无改变。16例IgE初始浓度≥200IU/ml者并发症较少,仪1例在完全性房室传导阻滞后出现休克,但存活。84例IgE初始浓度<200IU/ml者17例发生严重并发症,8例死亡。讨论一些作者认为嗜酸性细胞及其产物对AMI病裎有不利影响。已观察到AMI病人血清中具有细胞毒特性的嗜酸细胞阳离子蛋白升高。尸解也发现心脏破裂时比急性穿壁破裂时心肌坏死区嗜酸性细胞更多。但事实上本文15例第1周末嗜酸性细胞>300/mm~3者均无合并症。AMI早期IgE升高可能是机体对坏死组织释放的蛋白发生体液免疫的一部分。IgE可致敏肥大细胞释放化学介质;位于梗死带,表
The pathogenesis of coronary heart disease involves mast cells, which under the IgE-mediated mast cells can release a variety of vasoactive substances affect the local blood flow. Clinical data Serum IgE concentrations and blood eosinophil counts were determined by enzyme immunoassay in 100 patients with acute myocardial infarction (AMI) and 16 with acute coronary insufficiency (ACI) without evidence of AMI. Results After the AMI, the mean serum IgE concentration gradually increased, reached the peak on the 7th day, decreased on the 14th day and dropped to the normal level on the 3rd week. A small number of patients continued to decline. IgE increased while blood eosinophil count increased. ACI group IgE no change. 16 cases of IgE initial concentration of ≥ 200IU / ml less complications, the instrument in 1 case of shock after complete atrioventricular block, but survived. Of the 84 patients with IgE initial concentrations <200 IU / ml, 17 had serious complications and 8 died. Discussion Some authors believe that eosinophils and their products have a detrimental effect on AMI disease. Eosinophil cationic protein with cytotoxic properties has been observed to be elevated in the serum of AMI patients. An autopsy also found more eosinophils in the heart muscle necrosis area when the heart ruptured than when the acute transmural rupture. But in fact, 15 cases of the first weekend eosinophils> 300 / mm ~ 3 were no complications. Early elevated IgE in AMI may be part of the body’s humoral immunity to proteins released from necrotic tissue. IgE can sensitize mast cells to release chemical mediators; located in the infarct zone, the table