Lang S A, Maron M B
Department of Physiology, Northeastern Ohio Universities, College of Medicine, Rootstown 44272, USA.
J Appl Physiol (1985). 1998 Feb;84(2):618-23. doi: 10.1152/jappl.1998.84.2.618.
We evaluated the effect of neuropeptide Y (NPY) on the hemodynamics of the isolated rabbit lung perfused at constant flow and outflow pressure. Doses of 10(-8) and 10(-7) M NPY increased pulmonary arterial pressure (Ppa) from 11.5 +/- 1.0 (SE) mmHg to, respectively, 16.4 +/- 1.5 and 26.0 +/- 3.8 mmHg (P < 0.05, n = 5 mmHg lungs), with 78 +/- 4% of the increase at 10(-7) M resulting from an increased arterial resistance. At the latter dose, pulmonary capillary pressure increased from 5.8 +/- 0.9 to 9.4 +/- 1.0 mmHg (P < 0.05). When administered in the presence of norepinephrine, 10(-8) and 10(-7) M NPY (n = 6) produced extreme increases in Ppa to 66.1 +/- 20.5 and 114.7 +/- 25.5 mmHg, respectively, that were due primarily to an increased arterial resistance. To determine the significance of circulating NPY as a pulmonary vasoactive agent, we measured plasma NPY-like immunoreactivity in anesthetized rabbits after massively activating the sympathetic nervous system with veratrine. NPY-like immunoreactivity increased from 74 +/- 10 to 111 +/- 10 (SE) pM (P < 0.05). Thus, although NPY is a potent vasoconstrictor in the rabbit lung, it is not likely that plasma NPY concentrations rise sufficiently, even after massive sympathetic nervous system activation, to produce pulmonary vasoconstriction in the intact rabbit.
我们评估了神经肽Y(NPY)对以恒定流量和流出压力灌注的离体兔肺血流动力学的影响。剂量为10^(-8)和10^(-7) M的NPY可使肺动脉压(Ppa)分别从11.5±1.0(标准误)mmHg升高至16.4±1.5和26.0±3.8 mmHg(P<0.05,n = 5只肺),在10^(-7) M时,78±4%的升高是由于动脉阻力增加所致。在该剂量下,肺毛细血管压从5.8±0.9升高至9.4±1.0 mmHg(P<0.05)。当在去甲肾上腺素存在的情况下给药时,10^(-8)和10^(-7) M的NPY(n = 6)可使Ppa分别极度升高至66.1±20.5和114.7±25.5 mmHg,这主要是由于动脉阻力增加所致。为了确定循环NPY作为肺血管活性物质的意义,我们在用藜芦碱大量激活交感神经系统后,测量了麻醉兔血浆中NPY样免疫反应性。NPY样免疫反应性从74±10升高至111±10(标准误)pM(P<0.05)。因此,尽管NPY在兔肺中是一种有效的血管收缩剂,但即使在交感神经系统大量激活后,血浆NPY浓度也不太可能升高到足以在完整兔体内引起肺血管收缩的程度。