Rångemark C, Wennmalm A
Department of Clinical Physioogy, Göteborg University, Sweden.
Clin Physiol. 1996 May;16(3):301-15. doi: 10.1111/j.1475-097x.1996.tb00576.x.
The incidence of cigarette smoking tends to be higher in women, justifying directed studies on smoke-related mechanisms of cardiovascular disorder in females. Platelet activity plays an important etiological role in several settings of cardiovascular disease. Cigarette smoking facilitates platelet formation of proaggregatory thromboxane A2. However, cigarette smoke contains nitric oxide (NO), which has antiplatelet activity. Furthermore, the formation of anti-aggregatory prostacyclin (PGI2) may be higher in smokers than in non-smokers. Hence, the concerted action of NO and PGI2 on platelet activity in smoking females is important to elucidate. The metabolites of TxA2, NO, and PGI2, as well as cyclic guanosine 3':5'-monophosphate (cGMP; second messenger for NO in the platelets) and cyclic adenosine 3':5'-monophosphate (cAMP; second messenger for PGI2 in the platelets), were analysed in 23 healthy female smokers (daily consumption 11-20 cigarettes per day) and in 26 matched non-smokers. The urinary excretion of 2,3-dinor TxB2 (metabolite of TxA2) was considerably higher in smokers than in non-smokers (177 vs. 72 pg/mg creatinine, respectively; P<0.001). Plasma and urinary levels of nitrate (metabolite of inhaled NO) did not differ between the groups. Plasma and urinary cGMP were slightly increased (252 vs. 193 nmol/L; P<0.05 and 0.63 vs. 0.51 micromol/24 h; P<0.05, respectively) in smokers compared to non-smokers, while platelet cGMP was lower in smokers than in non-smokers (81 vs. 10.3 pmol/10(6) platelets, respectively; P<0.05). The urinary excretion of 2,3-dinor-6-keto-PGF1a (metabolite of PGI2) did not differ between the groups. Platelet or urinary cAMP did not differ between the groups either, while plasma cAMP was lower in smokers than in non-smokers (19.2 vs. 26.2 nmol/l, respectively; P<0.001). In healthy female smokers NO is not absorbed from the inhaled smoke, and endothelial PGI2 formation is not enhanced to counterbalance the increased platelet formation of proaggregatory TxA2.
女性吸烟的发生率往往较高，这使得针对女性心血管疾病与吸烟相关机制的定向研究具有合理性。血小板活性在多种心血管疾病的发病机制中起着重要作用。吸烟会促进血小板生成促聚集的血栓素A2。然而，香烟烟雾中含有一氧化氮（NO），其具有抗血小板活性。此外，吸烟者中抗聚集的前列环素（PGI2）的生成可能比不吸烟者更高。因此，阐明NO和PGI2对吸烟女性血小板活性的协同作用很重要。对23名健康女性吸烟者（每日吸烟11 - 20支）和26名匹配的非吸烟者的血栓素A2、NO和PGI2的代谢产物，以及环磷酸鸟苷（cGMP；血小板中NO的第二信使）和环磷酸腺苷（cAMP；血小板中PGI2的第二信使）进行了分析。吸烟者尿中2,3 - 二去甲血栓素B2（血栓素A2的代谢产物）的排泄量显著高于非吸烟者（分别为177 vs. 72 pg/mg肌酐；P<0.001）。两组之间血浆和尿中硝酸盐（吸入NO的代谢产物）水平无差异。与非吸烟者相比，吸烟者血浆和尿中的cGMP略有升高（分别为252 vs. 193 nmol/L；P<0.05和0.63 vs. 0.51 μmol/24 h；P<0.05），而吸烟者血小板中的cGMP低于非吸烟者（分别为81 vs. 10.3 pmol/10⁶血小板；P<0.05）。两组之间尿中2,3 - 二去甲 - 6 - 酮 - 前列环素F1a（前列环素I2的代谢产物）的排泄量无差异。两组之间血小板或尿中的cAMP也无差异，而吸烟者血浆中的cAMP低于非吸烟者（分别为19.2 vs. 26.2 nmol/L；P<0.001）。在健康女性吸烟者中，吸入烟雾中的NO未被吸收，并且内皮前列环素I2的生成未增强以抵消促聚集的血栓素A2血小板生成增加的影响。
