TNF-α has been shown to be a major factor responsible for myocardial depression during endotoxemia and cardiomyocytes are the major local source of TNF-α; however, so far few studies focus on the effect of propofol on cardiac function during endotoxemia or sepsis and no studies report whether propofol could inhibit LPS-induced TNF-α in cardiomyocytes [22, 23]. The gene discussed is TNF; the disease is serum lipopolysaccharide activity.