Winsö O, Biber B, Martner J
Acta Anaesthesiol Scand. 1985 Jul;29(5):508-14. doi: 10.1111/j.1399-6576.1985.tb02244.x.
Dopamine interference with intestinal and renal sympathetic reflex vasoconstrictor responses was studied in cats anaesthetized with diazepam, fentanyl and nitrous oxide. Vasoconstriction was induced by electric stimulation of the hypothalamic defence-alarm area and by stimulation of somatic and visceral afferents. In addition, intestinal vasoconstriction was elicited by direct stimulation of postganglionic sympathetic efferent nerves. In the intestine, dopamine administration (7.5 microgram X kg-1 X min-1) was not associated with an attenuation of the investigated sympathetic vasoconstrictor responses, although dopamine per se decreased intestinal vascular resistance by 36 +/- 4%. Due to this dopamine-induced background vasodilation, the intestinal blood flow level during stimulation procedures and concomitant dopamine infusion was higher than during similar stimulations prior to dopamine (for defence-alarm area stimulation 45 +/- 16%, for afferent nerve stimulation 79 +/- 22% and for efferent postganglionic nerve stimulation 66 +/- 16%). In the kidney, dopamine per se had only minor effects on vascular resistance and on changes in vascular tone elicited by the stimulation procedures. The renal blood flow level in response to the stimulation procedures was not significantly affected by dopamine. In conclusion, dopamine may contribute to a sustained intestinal blood flow level when administered during supervening stress-related sympathetic activation.
在用地西泮、芬太尼和一氧化二氮麻醉的猫身上,研究了多巴胺对肠道和肾脏交感神经反射性血管收缩反应的干扰作用。通过电刺激下丘脑防御警报区以及刺激躯体和内脏传入神经来诱导血管收缩。此外,通过直接刺激节后交感传出神经引发肠道血管收缩。在肠道中,给予多巴胺(7.5微克·千克⁻¹·分钟⁻¹)与所研究的交感神经血管收缩反应减弱无关,尽管多巴胺本身可使肠道血管阻力降低36±4%。由于多巴胺诱导的这种背景性血管舒张,在刺激过程中及同时输注多巴胺时的肠道血流水平高于多巴胺给药前类似刺激时的水平(防御警报区刺激时为45±16%,传入神经刺激时为79±22%,节后传出神经刺激时为66±16%)。在肾脏中,多巴胺本身对血管阻力以及刺激过程引起的血管张力变化影响较小。多巴胺对刺激过程所引起的肾血流水平无显著影响。总之,在伴随应激相关交感神经激活期间给予多巴胺时,它可能有助于维持肠道血流水平。