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首页> 外文期刊>Life sciences >Effect of neuropeptide Y on endotoxin-induced suppression of the response to various agonists in conscious rats.
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Effect of neuropeptide Y on endotoxin-induced suppression of the response to various agonists in conscious rats.

机译：神经肽Y对内毒素诱导的清醒大鼠对各种激动剂反应的抑制作用。

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Hypotension during endotoxic shock is related to reduced vascular responsiveness to vasoconstrictors. Neuropeptide Y (NPY) is known to potentiate the pressor response to some agonists, and NPY infusion has been shown to improve hemodynamics and survival in endotoxemic rats. We therefore studied the effect of NPY infusion on the suppressed pressor effect of norepinephrine (NE), angiotensin II (AII), vasopressin (VP), and endothelin (ET) in conscious endotoxemic rats. Chronically cannulated conscious rats were infused with a non-hypotensive dose of endotoxin (LPS, 10 micrograms/10 microliters/min) throughout the experiment. Infusion of NPY, 40 pmol/10 microliters/min was started 15 minutes before the LPS infusion, and continued for 65 minutes. Five minutes after the termination of NPY infusion, increasing agonist doses were administered i.v. to construct dose-response curves. Each experiment included one control group where saline replaced LPS, and one control group where saline replaced NPY. LPS infusion caused suppression of the pressor responses to all four agonists, as expressed by ED50 and by decreased pressor response to the individual agonist doses. In addition, LPS infusion altered the bradycardic response to AII and ET. NPY infusion prior to the administration of NE, AII and VP resulted in partial reversal of the LPS-induced suppressed responsiveness to these agonists. NPY infusion had no effect on the response to ET in either control or endotoxemic rats. Partial reversal of the suppressed responsiveness to the three agonists by NPY infusion may contribute to the observed NPY-induced improvement of blood pressure and survival rate during endotoxic shock.
机译：内毒素性休克期间的低血压与血管对血管收缩剂的反应性降低有关。已知神经肽Y（NPY）可以增强对某些激动剂的升压反应，并且已显示NPY输注可改善内毒素血症大鼠的血流动力学和存活率。因此，我们研究了有意识的内毒素血症大鼠中NPY输注对去甲肾上腺素（NE），血管紧张素II（AII），血管加压素（VP）和内皮素（ET）抑制升压作用的作用。在整个实验过程中，向慢性插管的清醒大鼠注入非降压剂量的内毒素（LPS，10微克/ 10微升/分钟）。在LPS输注前15分钟开始以40 pmol / 10微升/分钟的速度注入NPY，并持续65分钟。 NPY输注终止后五分钟，静脉内施用增加的激动剂剂量。绘制剂量反应曲线。每个实验包括一个对照组，用盐水代替LPS，和一个对照组，用盐水代替NPY。 LPS输注可抑制对所有四种激动剂的升压反应，如ED50所表达，以及对单个激动剂剂量的升压反应降低。此外，LPS输注改变了对AII和ET的心动过缓反应。在施用NE，AII和VP之前，NPY输注导致LPS诱导的对这些激动剂的抑制性反应的部分逆转。在对照组或内毒素血症大鼠中，NPY输注对ET的反应均无影响。 NPY输注对三种激动剂的抑制反应部分逆转可能有助于观察到的NPY诱导的内毒素休克期间血压和生存率的改善。

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