Grayson J, Oyebola D D
Br J Pharmacol. 1985 Aug;85(4):797-804. doi: 10.1111/j.1476-5381.1985.tb11078.x.
Resting blood flow, arterio-venous glucose and oxygen (A-V)O2 differences, glucose uptake and oxygen consumption by a segment of the upper jejunum were measured in anaesthetized dogs. Systemic arterial pressure was also measured. The effect of nicotine infusion (25 micrograms kg-1 i.v., over 10 min) on these measurements was recorded in untreated dogs, in dogs treated with propranolol (0.5 mg kg-1) to produce beta-adrenoceptor blockade and in dogs after alpha 1-adrenoceptor blockade with prazosin (0.2 mg kg-1). Nicotine cause a significant pressor response during infusion and a hypotensive response during the post infusion period. Propranolol did not significantly affect these results. Jejunal blood flow increased in the first half of nicotine infusion in both the untreated and beta-blocked animals. Vascular resistance was reduced during nicotine infusion and the decrease persisted post infusion in the beta-blocked group. In the untreated group (A-V)O2 was significantly reduced during the first 5 min of nicotine infusion, thereafter it returned to control levels, then rose significantly above control level, post infusion. beta-Adrenoceptor blockade had little effect on these responses to nicotine. When oxygen consumption was calculated it was found that nicotine had little effect during or after infusion. Nicotine caused significant hyperglycaemia during and for about 1 h after infusion. Tissue release of glucose was occasionally observed following the infusion. beta-Adrenoceptor blockade reduced the hyperglycaemia caused by nicotine. beta-Blockade alone increased uptake and nicotine caused a further three to four fold increase. Prazosin abolished the effects that were observed in the untreated and the alpha-blocked animals. 6 The present findings, related to our previous observations on the effects of catecholamines on glucose uptake by the bowel, are consistent with the hypothesis that nicotine has its action on bowel glucose uptake or release through its well-established action in releasing catecholamines and in activating beta-adrenoceptors. The responses are not related to oxygen utilization.
在麻醉犬身上测量了静息血流量、动静脉葡萄糖和氧(A-V)O₂差值、空肠上段一段的葡萄糖摄取和氧消耗。还测量了体循环动脉压。记录了尼古丁输注(25微克/千克静脉注射,持续10分钟)对这些测量值的影响,实验对象包括未治疗的犬、用普萘洛尔(0.5毫克/千克)治疗以产生β-肾上腺素能受体阻滞的犬以及用哌唑嗪(0.2毫克/千克)进行α₁-肾上腺素能受体阻滞后的犬。尼古丁在输注期间引起显著的升压反应,在输注后期间引起降压反应。普萘洛尔对这些结果没有显著影响。在未治疗和β-阻滞的动物中,尼古丁输注前半段空肠血流量增加。尼古丁输注期间血管阻力降低,在β-阻滞组中,这种降低在输注后持续存在。在未治疗组中,尼古丁输注的前5分钟内(A-V)O₂显著降低,此后恢复到对照水平,然后在输注后显著高于对照水平。β-肾上腺素能受体阻滞对尼古丁的这些反应影响很小。计算氧消耗时发现,尼古丁在输注期间或输注后影响很小。尼古丁在输注期间及输注后约1小时引起显著的高血糖。输注后偶尔观察到组织葡萄糖释放。β-肾上腺素能受体阻滞减轻了尼古丁引起的高血糖。单独的β-阻滞增加了葡萄糖摄取,尼古丁使其进一步增加三到四倍。哌唑嗪消除了在未治疗和α-阻滞动物中观察到的效应。6 本研究结果与我们先前关于儿茶酚胺对肠道葡萄糖摄取影响的观察结果相关,与以下假设一致:尼古丁通过其在释放儿茶酚胺和激活β-肾上腺素能受体方面的既定作用,对肠道葡萄糖摄取或释放产生作用。这些反应与氧利用无关。