Allen R A, Kluft C, Brommer E J
Eur J Clin Invest. 1984 Oct;14(5):354-61. doi: 10.1111/j.1365-2362.1984.tb01195.x.
The acute effect of cigarette smoking on the fibrinolytic enzyme system in blood was studied. It was found imperative to have an initial 30 min rest period, after venipuncture, to obtain a stable baseline in the fibrinolytic studies. The average heart rate, in inhaling smokers, increased from 64 to a peak of 79 beats min-1, 5-10 min after commencement of smoking. A peak in fibrinolytic activity was found to occur later, at 22.5 min. Analysis of the increase in fibrinolytic activity revealed no demonstrable activation of intrinsic systems via factor XII, nor changes in plasminogen, prekallikrein and C1-inactivator. No plasmin-alpha 2-antiplasmin complexes were detectable. The increase (P less than 0.01) was found to be due to extrinsic (tissue-type) plasminogen activator, revealed as C1-inactivator-resistant plasminogen activator activity, and further identified by quenching with anti-tissue plasminogen activator IgG. Thus, smoking appears to elicit a significant increase in the level of activity of circulating extrinsic plasminogen activator.
研究了吸烟对血液中纤维蛋白溶解酶系统的急性影响。发现在静脉穿刺后必须有一个初始30分钟的休息期,以便在纤维蛋白溶解研究中获得稳定的基线。吸入香烟的吸烟者,平均心率在开始吸烟后5 - 10分钟从64次/分钟增加到峰值79次/分钟。发现纤维蛋白溶解活性在22.5分钟后出现峰值。对纤维蛋白溶解活性增加的分析表明,未通过因子XII证实内源性系统的激活,也未发现纤溶酶原、前激肽释放酶和C1 - 灭活剂的变化。未检测到纤溶酶-α2-抗纤溶酶复合物。发现这种增加(P < 0.01)是由于外源性(组织型)纤溶酶原激活剂,表现为对C1 - 灭活剂有抗性的纤溶酶原激活剂活性,并通过用抗组织型纤溶酶原激活剂IgG淬灭进一步鉴定。因此,吸烟似乎会导致循环中外源性纤溶酶原激活剂的活性水平显著增加。