Nadler J L, Velasco J S, Horton R
Lancet. 1983 Jun 4;1(8336):1248-50. doi: 10.1016/s0140-6736(83)92698-3.
Urinary prostacyclin (PGI2) was measured in 12 chronic smokers and 12 non-smokers after inhalation of smoke from nicotine-containing and nicotine-free cigarettes. In a separate study a pressor dose of noradrenaline, which increases PGI2, was given to smokers and non-smokers. PGI2 was measured as the stable metabolite, 6-keto-PGF1 alpha in 4 h urine samples by radioimmunoassay after chromatography on LH-20 'Sephadex'. Smoking of nicotine-free cigarettes had no effect on PGI2 release in either smokers or non-smokers. In non-smokers inhalation of nicotine-containing tobacco smoke increased heart-rate, blood-pressure, and urine osmolality, but did not affect urinary 6-keto-PGF1 alpha. In contrast, when chronic smokers used nicotine-containing cigarettes there was a highly significant reduction in excretion of 6-keto-PGF1 alpha (192 +/- 20 to 138 +/- 17 ng/g creatinine). Noradrenaline increased PGI2 in non-smokers (181 +/- 16 to 348 +/- 56) but not in smokers. Smoking of nicotine-containing tobacco abolished the PGI2 response to noradrenaline. These observations suggest that inhalation of nicotine-containing tobacco smoke reduces vascular PGI2 production; this may be a factor in the development of accelerated cardiovascular disease.
在12名慢性吸烟者和12名非吸烟者吸入含尼古丁香烟和不含尼古丁香烟的烟雾后，对其尿中前列环素（PGI2）进行了测量。在另一项研究中，给吸烟者和非吸烟者注射了能增加PGI2的升压剂量去甲肾上腺素。通过在LH - 20“葡聚糖凝胶”上进行色谱分离后，采用放射免疫分析法在4小时尿液样本中测量作为稳定代谢产物的6 - 酮 - PGF1α来测定PGI2。吸不含尼古丁的香烟对吸烟者或非吸烟者的PGI2释放均无影响。在非吸烟者中，吸入含尼古丁的烟草烟雾会增加心率、血压和尿渗透压，但不影响尿中6 - 酮 - PGF1α。相反，当慢性吸烟者使用含尼古丁香烟时，6 - 酮 - PGF1α的排泄量显著降低（从192±20降至138±17 ng/g肌酐）。去甲肾上腺素可增加非吸烟者的PGI2（从181±16增至348±56），但对吸烟者无此作用。吸含尼古丁的烟草消除了PGI2对去甲肾上腺素的反应。这些观察结果表明，吸入含尼古丁的烟草烟雾会降低血管PGI2的生成；这可能是加速心血管疾病发展的一个因素。
