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
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发表时间:
1992
期刊:
影响因子:
--
通讯作者:
Pilati,CF
中科院分区:
文献类型:
--
作者:
Lang,SA;Maron,MB;Maender,KC;Pilati,CF
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.