Baxter G M, Moore J N, Tackett R L
Department of Large Animal Medicine, College of Veterinary Medicine, Athens, Georgia.
Equine Vet J. 1991 Jan;23(1):48-52. doi: 10.1111/j.2042-3306.1991.tb02713.x.
The in vitro responses of isolated vascular preparations of digital arteries and veins obtained from healthy anaesthetised horses were determined for dopamine and fenoldopam. The digital vessels were harvested, cut into 4 mm vascular segments, suspended in tissue baths and attached to force-displacement transducers. Dose-response studies between 10(-8) and 10(-4)M concentrations were performed for all drugs. The change in tension of each vascular ring was measured in grams of force. The reactivity between palmar and plantar digital vessels and baseline vascular responses were determined for dopamine. The vascular responses of dopamine were compared to in vitro data for other known vasoconstrictor agents. The mechanism of vasoconstriction induced by dopamine was further defined using prazosin, a specific competitive alpha-1 adrenoceptor antagonist. The vasodilating ability of fenoldopam, a dopamine-1 (DA-1) receptor agonist, was also determined using noradrenaline- preconstricted vascular segments from palmar digital vessels. The effective concentration to produce 50 per cent of the maximal response (EC50) and the maximal contraction in grams of force per milligram of the vascular ring (g/mg) were calculated. There were no differences in the reactivity between the palmar and plantar digital vessels. Dopamine produced intense constriction in arteries and veins but only at very high molar concentrations. Prazosin decreased significantly the sensitivity of the veins to dopamine (increased the mean EC50 values) but not the arteries. Prazosin had no effect on the maximal contractions of the vessels. Fenoldopam produced very little relaxation of either the arteries or veins. These results suggest that dopamine produces constriction in equine digital arteries and veins and that the constriction is only partially mediated by alpha-1 adrenoceptors.(ABSTRACT TRUNCATED AT 250 WORDS)
对从健康麻醉马匹获取的趾动脉和趾静脉的离体血管制剂进行了多巴胺和非诺多泮的体外反应测定。采集趾部血管，切成4毫米的血管段，悬挂于组织浴槽中并连接到力位移传感器。对所有药物进行了浓度在10(-8)至10(-4)M之间的剂量反应研究。每个血管环的张力变化以克力为单位进行测量。测定了掌侧和跖侧趾血管之间的反应性以及多巴胺的基线血管反应。将多巴胺的血管反应与其他已知血管收缩剂的体外数据进行了比较。使用特异性竞争性α-1肾上腺素能受体拮抗剂哌唑嗪进一步确定了多巴胺诱导血管收缩的机制。还使用来自掌侧趾血管的去甲肾上腺素预收缩血管段测定了多巴胺-1(DA-1)受体激动剂非诺多泮的血管舒张能力。计算了产生最大反应50%的有效浓度(EC50)以及每毫克血管环以克力为单位的最大收缩(g/mg)。掌侧和跖侧趾血管之间的反应性没有差异。多巴胺在动脉和静脉中产生强烈收缩，但仅在非常高的摩尔浓度下。哌唑嗪显著降低了静脉对多巴胺的敏感性(增加了平均EC50值)，但对动脉没有影响。哌唑嗪对血管的最大收缩没有影响。非诺多泮对动脉或静脉几乎没有舒张作用。这些结果表明，多巴胺在马的趾动脉和静脉中产生收缩，并且这种收缩仅部分由α-1肾上腺素能受体介导。(摘要截断于250字)
