Wennmalm A
Prostaglandins Med. 1979 Dec;3(6):321-6.
The hypothesis was investigated that cigarette smoking obstructs the blood flow response that develops as a protection against tissue damage in an organ subjected to ischemia (reactive hyperemia). Forearm blood flow was recorded at rest and following forearm ischemia before and after cigarette smoking in healthy male and female volunteers. The experiments were also repeated after pre-treatment of the subjects with indomethacin, a prostaglandin synthesis inhibitor. Before pre-treatment with indomethacin, ischemia induced a reactive hyperemia amounting to 20 +/- 4 ml/100 ml tissue. This hyperemia was significantly (p less than 0.01) reduced by cigarette smoking, to 12 +/- 3 ml/100 ml tissue. After indomethacin, which in itself lowered the reactive hyperemia to 8 +/- 2 ml/100 ml tissue, smoking did not elicit any effect. It is suggested that smoking counteracts reactive hyperemia in tissues by interfering with the same physiological mechanism as indomethacin, i.e. with the vascular formation of PG. The possible significance of this observation in relation to cigarette smoking and ischemic heart disease is stressed.
吸烟会阻碍在遭受缺血（反应性充血）的器官中作为组织损伤保护机制而产生的血流反应。在健康男性和女性志愿者中，记录了他们在吸烟前后静息状态下以及前臂缺血后的前臂血流情况。在受试者用前列腺素合成抑制剂吲哚美辛预处理后，重复了这些实验。在用吲哚美辛预处理之前，缺血会诱发反应性充血，达到20±4毫升/100毫升组织。吸烟使这种充血显著（p<0.01）减少至12±3毫升/100毫升组织。吲哚美辛本身会将反应性充血降低至8±2毫升/100毫升组织，在此之后，吸烟没有产生任何影响。研究表明，吸烟通过干扰与吲哚美辛相同的生理机制，即与血管中前列腺素的形成，来抵消组织中的反应性充血。强调了这一观察结果与吸烟和缺血性心脏病相关的可能意义。
