Bogaert M G, Schaepdryver A F, Willems J L
Br J Pharmacol. 1977 Feb;59(2):283-92. doi: 10.1111/j.1476-5381.1977.tb07491.x.
1 The dopamine-induced neurogenic vasodilation, previously described in the isolated perfused hindleg of the dog, has been studied in anaesthetized dogs with intact circulation in the hindleg. Dopamine was administered intravenously and/or intra-aortically, either as a bolus injection of 4 or 1l mug/kg, or as a continuous infusion of 4, 8, 16 or 32 mug kg-1 min-1. 2 Dopamine, given as a bolus injection or by infusion reversibly inhibited synaptic transmission in the paravertebral lumbar ganglia, studied with preganglionic stimulation at 1Hz. The inhibitory effect decreased gradually when the frequency of stimulation was increased to 16 Hz. The inhibition by dopamine was also present when spontaneous postganglionic activity was recorded. These effects were more pronounced on intra-aortic than on intravenous administration of dopamine. 3 In about half of the animals studied, injection or infusion of dopamine elicited a decrease of vascular resistance in the innervated femoral artery, whereas systemic blood pressure either did not change or decreased. In the denervated femoral artery, an increase in vascular resistance was alway observed. 4 The decrease in femoral vascular resistance was considered to correspond with neurogenic vasodilation caused by paravertebral ganglionic inhibition since (i) it only occurred in the innervated hindleg, (ii) blood pressure did not rise, (iii) this decrease was insensitive to atropine or propranolol and (iv) it was blocked by small doses of haloperidol. When hypovolemic shock was produced, the incidence of the neurogenic decrease of vascular resistance was smaller. 5 Dopamine also increased renal blood flow. This increase was not reduced by the occurrence of the neurogenic vasodilation in the inervated femoral artery. 6 These results are consistent with the idea that the dopamine-induced neurogenic vasodilation, originally described in the isolated perfused hindleg of the dog, also occurs when the circulation to the hindleg is intact. This suggests that, in the dog, also occurs when the circulation to the hindleg is intact. This suggests that, in the dog. the inhibitory effect of dopamine on sympathetic ganglia modulates its peripheral vasoconstrictor effects. In hypovolemic shock, where sympathetic nervous activity is high, the inhibitory effect of dopamine on sympathetic ganglia disappears and its direct vasoconstrictor effect on the vessels dominates.
先前在犬离体灌注后肢中所描述的多巴胺诱导的神经源性血管舒张，已在麻醉状态下后肢循环完整的犬身上进行了研究。多巴胺通过静脉内和/或主动脉内给药，给药方式为4或1μg/kg的单次推注，或4、8、16或32μg·kg⁻¹·min⁻¹的持续输注。
以单次推注或输注方式给予的多巴胺可逆性抑制腰旁神经节的突触传递，通过以1Hz的频率刺激节前神经来进行研究。当刺激频率增加到16Hz时，抑制作用逐渐减弱。当记录节后自发活动时，多巴胺的抑制作用也存在。与静脉内给予多巴胺相比，主动脉内给予多巴胺时这些效应更明显。
在大约一半的被研究动物中，注射或输注多巴胺会引起支配的股动脉血管阻力降低，而全身血压要么没有变化，要么降低。在去神经的股动脉中，总是观察到血管阻力增加。
股血管阻力的降低被认为与腰旁神经节抑制引起的神经源性血管舒张相对应，因为（i）它仅发生在有神经支配的后肢，（ii）血压没有升高，（iii）这种降低对阿托品或普萘洛尔不敏感，（iv）它被小剂量的氟哌啶醇阻断。当产生低血容量性休克时，神经源性血管阻力降低的发生率较小。
多巴胺还增加肾血流量。在有神经支配的股动脉中神经源性血管舒张的情况下，这种增加并未减少。
这些结果与以下观点一致，即最初在犬离体灌注后肢中描述的多巴胺诱导的神经源性血管舒张，在后肢循环完整时也会发生。这表明，在犬中，当后肢循环完整时也会发生。这表明，在犬中，多巴胺对交感神经节的抑制作用调节其外周血管收缩作用。在交感神经活动高的低血容量性休克中，多巴胺对交感神经节的抑制作用消失，其对血管的直接血管收缩作用占主导。
