Tong E Y, Mathé A A, Tisher P W
Am J Physiol. 1978 Dec;235(6):H803-8. doi: 10.1152/ajpheart.1978.235.6.H803.
Rabbit lungs were perfused via the pulmonary artery and norepinephrine (NE) measured in the outflows. The basal NE level was approximately 3 ng/min. Electrical stimulation (50 V, 1 ms, 10 Hz) of the sympathetic nerves doubled the NE release. Hexamethonium (10(-4) and 10(-5) M) had no effect on the release of NE. Administration of a monoamine oxidase (MAO) inhibitor, pargyline (70 mg/kg) resulted in a 20-fold NE increase by nerve stimulation, implying that the bulk of the amine does not reach the systemic circulation due to an active MAO. Methacholine (1 and 10 micrograms/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 micrograms/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PGE2 (100 ng/ml), but not PGS2alpha, (100 ng/ml), depressed NE release during nerve stimulation, whereas indomethacin (10 mg/kg) enhanced NE release before, during, and after nerve stimulation in seemingly normal animals. This indicates the existence of another presynaptic inhibitory mechanism for NE release in the lung: a PGE-mediated inhibition.
通过肺动脉对兔肺进行灌注，并测量流出液中的去甲肾上腺素（NE）。基础NE水平约为3 ng/分钟。对交感神经进行电刺激（50 V，1 ms，10 Hz）可使NE释放量增加一倍。六甲铵（10⁻⁴和10⁻⁵ M）对NE释放无影响。给予单胺氧化酶（MAO）抑制剂帕吉林（70 mg/kg）后，神经刺激导致NE增加了20倍，这意味着由于活跃的MAO，大部分胺未进入体循环。乙酰甲胆碱（1和10微克/毫升）通过神经刺激抑制NE释放。这种抑制作用被阿托品（5微克/毫升）消除。提示毒蕈碱抑制机制可能调节肺中NE的释放。前列腺素E2（100 ng/毫升）而非前列腺素S2α（100 ng/毫升）在神经刺激期间抑制NE释放，而吲哚美辛（10 mg/kg）在看似正常的动物中，在神经刺激之前、期间和之后均增强NE释放。这表明肺中NE释放存在另一种突触前抑制机制：前列腺素E介导的抑制。
