Toivanen J, Ylikorkala O, Viinikka L
Toxicol Appl Pharmacol. 1986 Feb;82(2):301-6. doi: 10.1016/0041-008x(86)90205-x.
We studied the effects of smoking and nicotine on the production of proaggregatory thromboxane A2 (TxA2), antiaggregatory prostacyclin (epoprostenol, PGI2), and on lipid peroxidation in vivo and in vitro. In the in vivo study, serum concentrations of thromboxane B2 (TxB2), a stable metabolite of TxA2, increased immediately after smoking three cigarettes but not after smoking the equivalent amount of tobacco in a pipe, whereas serum lipid peroxide values did not change in either group. In vitro, nicotine (2 X 10(-3) mol/liter) inhibited pulmonary TxB2 production by 70% and simultaneously stimulated the production of 6-keto-prostaglandin F1 alpha, a stable metabolite of PGI2, by 40%, which suggest that nicotine does not exert its effect at the cyclooxygenase level. During aggregation in platelet-rich plasma, TxB2 production was inhibited by 53% with 2 X 10(-3) mol/liter of nicotine, and during whole blood clotting the inhibition was 34% with 2 X 10(-4) mol/liter of nicotine. Thus the rise in cigarette smokers' serum TxB2 was probably caused by some constituent of cigarette smoke other than nicotine. The increased production of TxA2 following cigarette smoking may provide one explanation for the increased incidence of atherosclerosis and its complications in cigarette smokers.
我们研究了吸烟和尼古丁对体内和体外促聚集血栓素A2（TxA2）、抗聚集前列环素（依前列醇，PGI2）生成以及脂质过氧化的影响。在体内研究中，TxA2的稳定代谢产物血栓素B2（TxB2）的血清浓度在吸三支香烟后立即升高，但吸等量烟斗烟草后未升高，而两组的血清脂质过氧化物值均未改变。在体外，尼古丁（2×10⁻³摩尔/升）抑制肺TxB2生成70%，同时刺激PGI2的稳定代谢产物6-酮-前列腺素F1α生成40%，这表明尼古丁并非在环氧化酶水平发挥作用。在富含血小板血浆的聚集过程中，2×10⁻³摩尔/升尼古丁使TxB2生成受到53%的抑制，在全血凝血过程中，2×10⁻⁴摩尔/升尼古丁的抑制率为34%。因此，吸烟者血清TxB2升高可能是由香烟烟雾中除尼古丁之外的某些成分所致。吸烟后TxA2生成增加可能为吸烟者动脉粥样硬化及其并发症发病率升高提供一种解释。
