Archer S L, Kulik T J, Chesler E, Weir E K
Proc Soc Exp Biol Med. 1986 Oct;183(1):19-27. doi: 10.3181/00379727-183-42381.
Substance P is a vasoactive peptide. Nerve fibers containing substance P are present in the media of pulmonary arteries but the physiologic function of substance P in the pulmonary vasculature is unknown. Several doses of substance P were infused intravenously in the anesthetized dog to ascertain its effects on the pulmonary vasculature, both during normoxia and following preconstriction with hypoxia (F1O2 0.1) or prostaglandin F2 alpha (PGF2 alpha 5 mug/kg/min). Substance P resulted in systemic vasodilation during normoxia but had minimal effect on the pulmonary vasculature. During hypoxia and PGF2 alpha-induced pulmonary vasoconstriction, substance P significantly lowered pulmonary artery pressure, pulmonary vascular resistance, mean aortic pressure, and total systemic resistance. It had no effect on cardiac output, wedge pressure, and arterial blood gases. To investigate possible mechanisms for substance P-induced vasodilation, substance P was studied following pretreatment with N-acetylcysteine (a radical scavenging agent), methylene blue (an inhibitor of guanylate cyclase), meclofenamate (a cyclooxygenase inhibitor), and atropine (a muscarinic receptor antagonist). None of these agents impaired substance P-induced vasodilation. Substance P given intravenously is a nonselective vasodilator in the dog but the mechanism of its action remains uncertain.
P物质是一种血管活性肽。含有P物质的神经纤维存在于肺动脉中层，但P物质在肺血管系统中的生理功能尚不清楚。在麻醉犬身上静脉注射几剂P物质，以确定其在常氧期间以及在缺氧（F1O2 0.1）或前列腺素F2α（PGF2α 5微克/千克/分钟）预收缩后对肺血管系统的影响。P物质在常氧期间导致全身血管舒张，但对肺血管系统影响极小。在缺氧和PGF2α诱导的肺血管收缩期间，P物质显著降低肺动脉压、肺血管阻力、平均主动脉压和总全身阻力。它对心输出量、楔压和动脉血气无影响。为了研究P物质诱导血管舒张的可能机制，在使用N-乙酰半胱氨酸（一种自由基清除剂）、亚甲蓝（一种鸟苷酸环化酶抑制剂）、甲氯芬那酸（一种环氧化酶抑制剂）和阿托品（一种毒蕈碱受体拮抗剂）预处理后对P物质进行了研究。这些药物均未损害P物质诱导的血管舒张。静脉注射的P物质在犬体内是一种非选择性血管舒张剂，但其作用机制仍不确定。
