Wennmalm A
Br J Pharmacol. 1977 Jan;59(1):95-100. doi: 10.1111/j.1476-5381.1977.tb06981.x.
Rabbit isolated hearts were perfused according to Langendorff with Tyrode solution. Prostaglandin-like substances (PLS) in the effluent were purified and assayed on the rat stomach strip Noradrenaline (NA) in the effluent was assayed fluorimetrically. 2 Infusion of nicotine (1 muM-50 muM) caused a dose-dependent, brief increase, from 1.2+/-0.4 to maximally 8.3+/-2.1 ng/min, in the outflow of PLS from the heart. The increase was abolished by pretreatment of the heart with indomethacin. 3 Activation of nicotinic receptors in the heart with acetylcholine (ACh, 200 muM) in the presence of atropine (1 muM) also elicited an increase in the release of PLS. This release was smaller than that caused by nicotine. 4 Nicotine (50 muM) and ACh (200 muM) in the presence of atropine (1 muM) each caused a pronounced but brief release of NA into the effluent. There was no evident correlation between the ability of the drugs to cause release of PLS on the one hand, and NA on the other. 5 It is concluded that nicotine acts as a direct stimulus for the synthesis of prostaglandins in the rabbit heart.
兔离体心脏按Langendorff法用台氏液灌注。流出液中的前列腺素样物质(PLS)被纯化,并在大鼠胃条上进行测定。流出液中的去甲肾上腺素(NA)用荧光法测定。2. 注入尼古丁(1μM - 50μM)导致心脏流出液中PLS的流出量呈剂量依赖性短暂增加,从1.2±0.4 ng/min最大增加到8.3±2.1 ng/min。吲哚美辛预处理心脏可消除这种增加。3. 在阿托品(1μM)存在的情况下,用乙酰胆碱(ACh,200μM)激活心脏中的烟碱受体也会引起PLS释放增加。这种释放比尼古丁引起的释放小。4. 在阿托品(1μM)存在的情况下,尼古丁(50μM)和乙酰胆碱(200μM)各自都会导致明显但短暂的NA释放到流出液中。药物引起PLS释放的能力与引起NA释放的能力之间没有明显的相关性。5. 得出结论,尼古丁是兔心脏中前列腺素合成的直接刺激物。