Central alpha 2-adrenergic control of the pattern of small intestinal motility in rats.
Central alpha 2-adrenergic control of the pattern of small intestinal motility in rats.
复制标题
中枢α2-肾上腺素能控制大鼠小肠运动模式。
作者：
M. Fargeas;J. Fioramonti;L. Buéno
在长期装有植入十二指肠空肠壁的电极和放置在大脑侧脑室的插管的清醒大鼠中，检查中枢和外周施用α2-肾上腺素受体激动剂和拮抗剂对小肠运动的影响。在禁食的大鼠中，脑室内或腹膜内给予可乐定（5微克）立即破坏了迁移性肌电复合体模式，在第一个小时内完全抑制了尖峰活动，随后是一段持续2小时的不规则尖峰活动。先前肌肉注射育亨宾（600微克）可消除抑制作用，脑室内注射育亨宾（30微克）可抑制不规则活动期。萘甲唑啉是一种很难穿过血脑屏障的 α2 激动剂，仅在腹膜内给药（1 微克）时抑制尖峰活动，而在脑室内以相同剂量给药时仅诱导一段不规则的尖峰活动。在喂食的大鼠中，脑室内给予育亨宾或酚妥拉明（30微克），以及较小程度的哌唑嗪，可恢复禁食状态下典型的迁移肌电复合模式。这三种拮抗剂以20倍高的剂量外周给药是无效的。最后，α2-激动剂的喂养和中枢给药都会破坏肌电复合体的迁移模式。这些药理学数据表明中枢α2-肾上腺素受体在调节大鼠肠道蠕动中可能发挥作用。
The effects of central and peripheral administration of alpha 2-adrenoceptor agonists and antagonists on small intestinal motility were examined in conscious rats chronically fitted with electrodes implanted in the duodenojejunal wall and a cannula placed in a cerebral lateral ventricle. In fasted rats, intracerebroventricular or intraperitoneal administration of clonidine (5 micrograms) immediately disrupted the migrating myoelectric complex pattern with a total inhibition of spiking activity during the first hour, followed by a period of irregular spiking activity for 2 h. The inhibition was abolished by previous intramuscular administration of yohimbine (600 micrograms), and the period of irregular activity was suppressed by intracerebroventricular yohimbine (30 micrograms). Naphazoline, an alpha 2-agonist that poorly crosses the blood-brain barrier, only inhibited spiking activity when administered intraperitoneally (1 microgram) and induced only a period of irregular spiking activity when administered intracerebroventricularly at the same dose. In fed rats, intracerebroventricular administration of yohimbine or phentolamine (30 micrograms), and to a lesser extent prazosin, restores a migrating myoelectric complex pattern typical of the fasted state. Peripheral administration of these three antagonists at a dose 20 times higher was ineffective. Finally, both feeding and central administration of alpha 2-agonists disrupt the migrating myoelectric complex pattern. Such pharmacologic data suggest a possible role of central alpha 2-adrenoceptors in the regulation of intestinal motility in rats.