Circulating neuropeptide Y does not produce pulmonary hypertension during massive sympathetic activation.

Circulating neuropeptide Y does not produce pulmonary hypertension during massive sympathetic activation.
复制标题

循环神经肽 Y 在大量交感神经激活期间不会产生肺动脉高压。

DOI:
10.1152/jappl.1992.73.1.117
复制
发表时间:
1992
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Pilati,CF
Pilati,CF
中科院分区:
--
文献类型:
--
作者:
Lang,SA;Maron,MB;Maender,KC;Pilati,CF

文献摘要

被引文献

相似文献

我们测试了神经肽Y (NPY)可能导致氯氯糖麻醉的狗在内胆给药缬草碱产生大量交感神经激活后出现肺动脉高压的可能性。在6只狗中,缬草碱引起动脉npy样免疫反应性(NPY-LI)在60-120分钟内从873 +/- 150 (SE) pg/ml上升到峰值3780 +/- 666 pg/ml。(在3只动物中,肾上腺切除术显著降低了NPY-LI的升高。)在另外5只狗中,我们注射猪NPY 30分钟,其剂量使动脉NPY- li增加到8,354 +/- 1,514 pg/ml,并观察到肺血流动力学仅发生轻微变化。在三种离体犬左下肺叶灌注(LLL)制剂中,增加NPY的剂量,在最高剂量时产生血浆NPY- li水平,超过给药后观察到的水平三个数量级。在任何剂量下均未观察到LLL动脉或双闭塞毛细血管压力的变化。同样,在输注去甲肾上腺素的同时给予NPY,另外三个脑叶的LLL血流动力学没有变化。我们得出结论,NPY不太可能作为循环血管活性物质在该模型中产生肺动脉高压和水肿中起作用。
We tested the possibility that neuropeptide Y (NPY) may contribute to the pulmonary hypertension that occurs after massive sympathetic activation produced by intracisternal veratrine administration in the chloralose-anesthetized dog. In six dogs, veratrine caused arterial NPY-like immunoreactivity (NPY-LI) to rise from 873 +/- 150 (SE) pg/ml to peak values of 3,780 +/- 666 pg/ml by 60–120 min. (In 3 animals, adrenalectomy significantly reduced the increases in NPY-LI.) In five additional dogs, we infused porcine NPY for 30 min in doses that increased arterial NPY-LI to 8,354 +/- 1,514 pg/ml and observed only minor changes in pulmonary hemodynamics. In three isolated perfused canine left lower lung lobe (LLL) preparations, increasing doses of NPY were administered, producing levels of plasma NPY-LI, at the highest dose, that exceeded those observed after veratrine administration by three orders of magnitude. No changes in LLL arterial or double-occlusion capillary pressures were observed at any dose. Similarly, no changes in LLL hemodynamics were observed in three additional lobes when NPY was administered while norepinephrine was being infused. We conclude that it is unlikely that NPY plays a role as a circulating vasoactive agent in producing the pulmonary hypertension and edema that occur in this model.