Willette R N, Sapru H N
Eur J Pharmacol. 1982 Feb 19;78(1):61-70. doi: 10.1016/0014-2999(82)90372-7.
The administration of [D-Ala2,Met5]enkephalinamide (D-AME) and [D-Ala2,Leu5]enkephalinamide (D-ALE) into the right atrium of decerebrate rats caused bradycardia, a slight transient biphasic blood pressure response and apnea within 1-2 sec. Apnea was followed by rapid shallow breathing. These effects were dose related (1-1000 micrograms/kg) and blocked by pretreatment with naloxone. Atropine blocked the bradycardia. Sectioning the vagi at the level of the diaphragm did not affect the responses, whereas bivagotomy below the cardiac branches abolished all responses. The triad of responses was attributed to a reflex action arising from vagal afferents within the lung. These results were confirmed in paralyzed , artificially ventilated animals. In these animals, the enkephalin analogues produced a cessation of phrenic nerve (PN) activity followed by a decrease in the duration of bursts. The recurrent laryngeal nerve (RLN) was concomitantly excited in a continuous decremental fashion. This excitation was independent of PN inhibition. Recordings of single and near single pulmonary vagal afferents demonstrated no effect of D-AME or D-ALE on stretch and irritant receptors. However, type J-receptors were stimulated.
将[D-丙氨酸2，甲硫氨酸5]脑啡肽酰胺（D-AME）和[D-丙氨酸2，亮氨酸5]脑啡肽酰胺（D-ALE）注入去大脑大鼠的右心房，1-2秒内可引起心动过缓、轻微短暂的双相血压反应及呼吸暂停。呼吸暂停后紧接着是快速浅呼吸。这些效应呈剂量相关（1-1000微克/千克），且可被纳洛酮预处理所阻断。阿托品可阻断心动过缓。在横膈膜水平切断迷走神经并不影响反应，而在心脏分支以下进行双侧迷走神经切断则消除了所有反应。这三联反应归因于肺内迷走神经传入纤维产生的反射作用。这些结果在麻痹、人工通气的动物中得到了证实。在这些动物中，脑啡肽类似物使膈神经（PN）活动停止，随后爆发持续时间缩短。喉返神经（RLN）同时以持续递减的方式被兴奋。这种兴奋与PN抑制无关。对单个和近乎单个肺迷走神经传入纤维的记录表明，D-AME或D-ALE对牵张和刺激感受器无影响。然而，J型感受器受到了刺激。
