Sjövall H
Acta Physiol Scand Suppl. 1984;535:1-63.
The study was performed to test the hypothesis that the sympathetic nerves to the small intestine might be involved in the feed-back control of extra-cellular fluid volume. In a series of experiments in anaesthetized cats, we studied how efferent stimulation of the splanchnic nerves affected jejunal fluid transport rate. The mechanisms behind the observed responses were analysed and we also attempted to determine the physiological role of the sympathetic supply to the jejunal mucosa. Splanchnic nerve stimulation (SNS) led to an increase in net fluid absorption provided that glucose was present in the jejunal lumen. In segments exposed to cholera toxin, SNS had a very pronounced inhibitory effect on net fluid secretion. The absorptive response was significant at a stimulation rate of 2 Hz and the maximal response occurred at 4-8 Hz. The effect was blocked by phentolamine, an alpha-adrenergic antagonist, and it was mimicked by a close intraarterial infusion of noradrenaline, an alpha-adrenergic agonist. The absorptive response to SNS was still present after blockade of the intestinal vasoconstrictor nerves with hexamethonium, indicating that the sympathetic pathways to the epithelium and to vascular smooth muscle may employ different ganglionic transmitter mechanisms. The increase in net fluid absorption induced by SNS was due to the inhibition of a secretory process. The response was not secondary to changes in intestinal blood flow. The effect of noradrenaline infusion was abolished after blockade of the intestinal nerves with tetrodotoxin, a finding which indicates that the sympathetic nerves may act by modulation of the activity in intramural secretory nervous pathways. Unloading of carotid sinus baroreceptors led to an increase in jejunal fluid absorption, a response which was abolished by division of the sympathetic fibres to the segment. Unloading of cardiac mechanoreceptors enhanced jejunal fluid absorption or decreased cholera secretion, effects which were abolished by previous cervical vagotomy or local alpha-adrenoreceptor blockade of the jejunal segment. Afferent stimulation of the right cardiac nerve led to an inhibition of net fluid absorption if the nerve was stimulated with high-threshold parameters at frequencies below 1 Hz.
支配小肠的交感神经可能参与细胞外液量的反馈控制。在一系列针对麻醉猫的实验中,我们研究了内脏神经的传出刺激如何影响空肠液转运速率。分析了观察到的反应背后的机制,并且我们还试图确定交感神经对空肠黏膜供应的生理作用。只要空肠腔内存在葡萄糖,内脏神经刺激(SNS)就会导致净液体吸收增加。在暴露于霍乱毒素的节段中,SNS对净液体分泌有非常明显的抑制作用。在2Hz的刺激频率下吸收反应显著,最大反应出现在4 - 8Hz。该效应被α - 肾上腺素能拮抗剂酚妥拉明阻断,并且被α - 肾上腺素能激动剂去甲肾上腺素的动脉内近距离输注模拟。用六甲铵阻断肠血管收缩神经后,对SNS的吸收反应仍然存在,这表明通向肠上皮和血管平滑肌的交感神经通路可能采用不同的神经节递质机制。SNS引起的净液体吸收增加是由于分泌过程的抑制。该反应并非继发于肠血流量的变化。用河豚毒素阻断肠神经后,去甲肾上腺素输注的效应消失,这一发现表明交感神经可能通过调节壁内分泌神经通路的活动起作用。颈动脉窦压力感受器去负荷导致空肠液吸收增加,该反应在切断支配该节段的交感纤维后消失。心脏机械感受器去负荷增强空肠液吸收或减少霍乱分泌,这些效应在先前的颈迷走神经切断术或空肠节段局部α - 肾上腺素能受体阻断后消失。如果以低于1Hz的高阈值参数刺激右心神经,其传入刺激会导致净液体吸收受到抑制。