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某些α-肾上腺素能受体激动剂和阻滞剂对家兔唾液淀粉酶分泌的影响。

Effects of some alpha-adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit.

作者信息

Gjörstrup P

出版信息

Acta Physiol Scand. 1984 Apr;120(4):567-77. doi: 10.1111/j.1748-1716.1984.tb07422.x.

Abstract

In rabbits under urethane anaesthesia parotid secretion of fluid and amylase in response to electrical stimulation of the sympathetic and parasympathetic nerves was measured before and after injections of various agents acting on alpha-adrenoceptors. Amylase secretion in response to sympathetic nerve stimulation at 0.5 and 1 Hz was markedly reduced by clonidine, 0.5-30 micrograms/kg, in a dose related manner. The effect was not due to an altered responsiveness of the gland, since isoprenaline still caused a large release of amylase. Phenylephrine, 10 micrograms/kg, and prazosine, 300 micrograms/kg, had no effect on the sympathetically evoked amylase secretion. Yohimbine in a dose of 0.5 mg/kg increased the amylase output in response to sympathetic nerve stimulation at 0.5 Hz by 70%, while the response at 1 Hz, which is close to maximum for the gland, was not significantly increased. The fluid and amylase secretion produced by parasympathetic nerve stimulation at 1.5, 5.0 and 10 Hz remained unchanged after clonidine, 1.0-30 micrograms/kg, or yohimbine 0.5 mg/kg. In rabbits provided with chronic parotid fistulae fluid and amylase secretion were studied after injections of clonidine, 30 micrograms/kg, and yohimbine, 1 mg/kg. In the conscious animal clonidine reduced not only amylase but also fluid secretion, by around 50 and 30%, respectively, indicating an effect on the activity in both the sympathetic and parasympathetic secretory nerves. Yohimbine increased the output of amylase during feeding, seen as an increased mean output of amylase due to an increased concentration of amylase in the saliva, while fluid secretion remained unchanged. The various experiments suggest that amylase secretion in response to sympathetic activation may be influenced by prejunctional control of transmitter release via alpha-2-adrenoceptors, and that this control may be of physiological significance. Parasympathetically evoked secretion does not seem to be under the influence of a similar control.

摘要

在氨基甲酸乙酯麻醉的家兔中,在注射各种作用于α-肾上腺素能受体的药物前后,测量了腮腺对交感神经和副交感神经电刺激的液体和淀粉酶分泌。可乐定(0.5 - 30微克/千克)以剂量相关的方式显著降低了0.5赫兹和1赫兹交感神经刺激引起的淀粉酶分泌。这种作用并非由于腺体反应性改变,因为异丙肾上腺素仍能引起大量淀粉酶释放。10微克/千克的去氧肾上腺素和300微克/千克的哌唑嗪对交感神经诱发的淀粉酶分泌没有影响。0.5毫克/千克的育亨宾使0.5赫兹交感神经刺激引起的淀粉酶输出增加了70%,而在1赫兹(接近腺体最大反应频率)时的反应没有显著增加。1.0 - 30微克/千克的可乐定或0.5毫克/千克的育亨宾对1.5、5.0和10赫兹副交感神经刺激产生的液体和淀粉酶分泌没有影响。在有慢性腮腺瘘管的家兔中,注射30微克/千克的可乐定和1毫克/千克的育亨宾后,研究了液体和淀粉酶分泌。在清醒动物中,可乐定不仅使淀粉酶分泌减少,也使液体分泌减少,分别约为50%和30%,表明对交感和副交感分泌神经的活动均有影响。育亨宾增加了进食期间的淀粉酶输出,表现为由于唾液中淀粉酶浓度增加导致淀粉酶平均输出增加,而液体分泌保持不变。各种实验表明,交感神经激活引起的淀粉酶分泌可能受通过α₂ - 肾上腺素能受体对递质释放的突触前控制的影响,并且这种控制可能具有生理意义。副交感神经诱发的分泌似乎不受类似控制的影响。

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