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自主神经系统在急性给予吗啡的免疫抑制作用中的潜在作用。

Potential role of the autonomic nervous system in the immunosuppressive effects of acute morphine administration.

作者信息

Flores L R, Dretchen K L, Bayer B M

机构信息

Department of Pharmacology, Georgetown University Medical Center, Washington, DC 20007, USA.

出版信息

Eur J Pharmacol. 1996 Dec 30;318(2-3):437-46. doi: 10.1016/s0014-2999(96)00788-1.

Abstract

These studies investigated the role of the autonomic nervous system in mediating the immunosuppressive effect of morphine on blood lymphocyte proliferation in rats. To determine the contribution of the autonomic nervous system, rats were pretreated with the ganglionic blocker chlorisondamine (5 mg/kg) prior to morphine (7 mg/kg) administration. Ganglionic blockade with chlorisondamine completely antagonized the inhibitory actions of morphine, suggesting that intact ganglionic transmission was required for the inhibition to occur. Blockade of postganglionic parasympathetic neurotransmission with atropine methylbromide (1 mg/kg) or blockade of sympathetic neurotransmission with the alpha-adrenoceptor antagonist phentolamine (1 mg/kg) did not attenuate the suppressive effect of morphine. Blockade of beta-adrenoceptors with propranolol (2.5 mg/kg) resulted in partial antagonism, but this action was not shared by the peripherally acting beta-adrenoceptor antagonist nadolol (6 mg/kg). These results suggest that the inhibitory effect of morphine on blood lymphocyte proliferation may be mediated through activation of the autonomic nervous system; however, individual blockade of either the parasympathetic or sympathetic division of the autonomic nervous system was not sufficient to antagonize this immunosuppressive effect.

摘要

这些研究调查了自主神经系统在介导吗啡对大鼠血液淋巴细胞增殖的免疫抑制作用中的作用。为了确定自主神经系统的作用,在给予吗啡(7毫克/千克)之前,先给大鼠注射神经节阻滞剂氯异吲哚铵(5毫克/千克)进行预处理。氯异吲哚铵引起的神经节阻断完全拮抗了吗啡的抑制作用,这表明完整的神经节传递是产生这种抑制作用所必需的。用甲基溴化阿托品(1毫克/千克)阻断节后副交感神经传递或用α-肾上腺素能受体拮抗剂酚妥拉明(1毫克/千克)阻断交感神经传递,均未减弱吗啡的抑制作用。用普萘洛尔(2.5毫克/千克)阻断β-肾上腺素能受体导致部分拮抗作用,但外周作用的β-肾上腺素能受体拮抗剂纳多洛尔(6毫克/千克)没有这种作用。这些结果表明,吗啡对血液淋巴细胞增殖的抑制作用可能是通过自主神经系统的激活来介导的;然而,单独阻断自主神经系统的副交感或交感分支不足以拮抗这种免疫抑制作用。

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