Pulmonary opiate receptor activation evokes a cardiorespiratory reflex.
Pulmonary opiate receptor activation evokes a cardiorespiratory reflex.
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肺阿片受体激活引起心肺反射。
DOI：
10.1016/0014-2999(82)90372-7
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发表时间：
1982
影响因子：
5
通讯作者：
Sapru,HN
中科院分区：
文献类型：
--
作者：
Willette,RN;Sapru,HN
将[D-Ala2,Met5]脑啡酰胺(D-AME)和[D-Ala2,Leu5]脑啡酰胺(D-ALE)注入去大脑大鼠的右心房会在1-2秒内引起心动过缓、轻微的短暂双相血压反应和呼吸暂停。呼吸暂停之后是快速浅呼吸。这些效应与剂量相关（1-1000 μg/kg），并可通过纳洛酮预处理来阻断。阿托品可阻断心动过缓。在膈肌水平处切断迷走神经并不影响反应，而在心脏分支下方进行双迷走神经切断术则消除了所有反应。这三联反应归因于肺内迷走神经传入引起的反射作用。这些结果在瘫痪的人工通气动物身上得到了证实。在这些动物中，脑啡肽类似物导致膈神经（PN）活动停止，随后爆发持续时间减少。喉返神经（RLN）同时以连续递减的方式兴奋。这种兴奋与 PN 抑制无关。单个和近单个肺迷走神经传入的记录表明 D-AME 或 D-ALE 对牵张和刺激受体没有影响。然而，J 型受体受到刺激。
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 μg/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 affarents demonstrated no effect of D-AME or D-ALE on stretch and irritant receptors. However, type J-receptors were stimulated.