Imai T, Takase S, Arai M, Fujita T
Jpn Circ J. 1983 Mar;47(3):289-93. doi: 10.1253/jcj.47.289.
Although some studies suggest the involvement of a complement activation in the development of acute myocardial infarction, there has been little convincing evidence of the change of the complement in patients suffering from myocardial infarction. In 11 patients with acute myocardial infarction the serial changes of the total hemolytic complement titer (CH50), C3, C4, total serum protein and C3 conversion were investigated up to 120 hours after its attack. The level of CH50 and C4 increased consistently in the acute phase of myocardial infarction, but C3 did not show any change and total serum protein declined after 96 hours. Beta 1 A globulin, the split product of C3, could not be detected in the blood stream. These results suggest that the infarcted or ischemic myocardium would activate complements, and C3 might be consumed continuously by the infarcted or ischemic myocardium. Such consumption of complements should stimulate the production of complement and would give rise of an increase in C4 and CH50. It is suggested that activated complement might play a significant role in the development of myocardial infarction.
尽管一些研究表明补体激活参与急性心肌梗死的发展过程，但几乎没有令人信服的证据表明心肌梗死患者补体发生了变化。对11例急性心肌梗死患者在发病后120小时内进行了总溶血补体滴度（CH50）、C3、C4、总血清蛋白及C3转化的系列变化研究。心肌梗死急性期CH50和C4水平持续升高，但C3无变化，96小时后总血清蛋白下降。血流中未检测到C3的裂解产物β1A球蛋白。这些结果提示梗死或缺血心肌可激活补体，梗死或缺血心肌可能持续消耗C3。补体的这种消耗应刺激补体产生，导致C4和CH50升高。提示激活的补体可能在心肌梗死的发展中起重要作用。
