Uchida Y, Masuo M, Sugimoto T
Jpn Heart J. 1986 Nov;27(6):839-48. doi: 10.1536/ihj.27.839.
PG I2 stimulating plasma factor was measured in patients with ischemic heart disease and age-matched controls. The plasma factor measured by bioassay using rat aorta was 3.2 +/- 0.6 (n = 21), 2.7 +/- 0.8 (n = 7), 1.6 +/- 1.5*** (n = 18) and 2.2 +/- 0.06** (n = 3) PG I2 ng/mg rat aorta (mean +/- SD; * p less than 0.05, ** p less than 0.01, *** p less than 0.001) in control, angina pectoris, acute myocardial infarction and old myocardial infarction with angina pectoris groups, respectively. The plasma factor measured by radioimmunoassay was 43.5 +/- 19.5 (n = 11), 35.4 +/- 13.1 (n = 4), 38.5 +/- 18.0 (n = 9), 26.0 +/- 20.1* (n = 7) and 59.5 +/- 31.2 (n = 5) ng/mg rat aortic protein/15 min in control, variant angina, stable angina, acute myocardial infarction and old myocardial infarction groups, respectively. The factor in deproteinized plasma of the acute myocardial infarction group was also smaller than that of the control group. PG I2 synthesis by rat aortic ring was inhibited by mepacrine, which inhibits phospholipase A2. The plasma factor was not inactivated by heating. The results indicate that a heat-stable plasma factor which acts on phospholipase A2 or on its surrounding reaction systems is deficient in the early stage of acute myocardial infarction. A decrease in the factor may cause PG I2 deficiency, resulting in coronary thrombosis or vasospasm and consequently in acute myocardial infarction.
对缺血性心脏病患者和年龄匹配的对照组测定了前列环素（PG I2）刺激血浆因子。采用大鼠主动脉生物测定法测得的血浆因子在对照组、心绞痛组、急性心肌梗死组和伴有心绞痛的陈旧性心肌梗死组中分别为3.2±0.6（n = 21）、2.7±0.8（n = 7）、1.6±1.5***（n = 18）和2.2±0.06**（n = 3）PG I2 ng/mg大鼠主动脉（均值±标准差；*p＜0.05，**p＜0.01，**p＜0.001）。采用放射免疫测定法测得的血浆因子在对照组、变异型心绞痛组、稳定型心绞痛组、急性心肌梗死组和陈旧性心肌梗死组中分别为43.5±19.5（n = 11）、35.4±13.1（n = 4）、38.5±18.0（n = 9）、26.0±20.1（n = 7）和59.5±31.2（n = 5）ng/mg大鼠主动脉蛋白/15分钟。急性心肌梗死组去蛋白血浆中的该因子也低于对照组。抑制磷脂酶A2的米帕林可抑制大鼠主动脉环合成PG I2。该血浆因子加热后未失活。结果表明，一种作用于磷脂酶A2或其周围反应系统的热稳定血浆因子在急性心肌梗死早期缺乏。该因子减少可能导致PG I2缺乏，进而引起冠状动脉血栓形成或血管痉挛，最终导致急性心肌梗死。
