心衰中的炎症ppt课件幻灯（英文）.pptVIP

Inflammation in heart failure;;Inflammation and Heart failure;β-adrenergic stimulation induces proinflammatory cytokine expression in myocardium;Causal relationship between Ang II and TGF-β1 in cardiac hypertrophy;Evidence for a connection between Ang II and TGF-β1 in cardiac tissue;Angiotensin II-induced myocardial TNF biosynthesis in the adult heart ;Angiotensin II induced activation of NF-?B;Cross-regulation between the renin-angiotensin system andinflammatory mediators;Inflammation and Heart failure;Autoimmune response after AMI;New field of therapy in inflammation and heart failure;Myocardial inflammation should be suppressed or regulated after AMI?;New field of therapy in inflammation and heart failure;RENEWAL trial;Explanations by designer;ATTACH trial;ATTACH trial results;The activation of TNF-α may not play a deleterious role in heart failure The toxicity of TNF-α might be also enhanced if treatment with infliximab caused circulating levels of TNF-α to rebound When exposed to cells expressing transmembrane TNF-α, infliximab can cause cell lysis in the presence of complement;Expression of cytokines in myocardium after AMI;RENEWAL trial: The doses of etanercept may be sufficient to neutralize circulating TNF-α, but not sufficient to neutralize myocardial TNF-α ATTACH trial: Infliximab is directly cytotoxic to cells expressing TNF-α on the myocardium. So high doses of infliximab (10mg/kg) adversely affected the clinical condition of patients with chronic heart failure. The anti-cytokine therapy is aborted because the cytokines might be secreted by means of an autocrine and paracrine in myocardium;New field of therapy in inflammation and heart failure ; Carvedilol reduced cardiac cytokine protein expression in AMI rats after therapy 4w ;Carvedilol decreased myocardial MMP-2 and MMP-9 expression in AMI rats;Carvedilol decreased myocardial type Ⅰand Ⅲ collagens expression in AMI rats (200×);Metoprolol regulates cytokines protein production of LV myocardium po