Richardson P D, Withrington P G
Eur J Pharmacol. 1978 Apr 15;48(4):337-49. doi: 10.1016/0014-2999(78)90160-7.
Dopamine was injected in graded doses into the hepatic artery of the anaesthetized dog: the typical response was an initial vasoconstriction followed by a more protracted vasodilatation. The vasodilatation was unaffected by propranolol, but was antagonized by haloperidol. The initial hepatic arterial vasoconstriction was inhibited both by haloperidol and by phentolamine. The experiments suggest that the initial vasoconstriction was due to alpha-adrenoceptor stimulation and that the secondary vasodilatation was the result of the stimulation of dopamine receptors. In separate experiments, dopamine was injected into the hepatic portal vein of the dog. The only response seen was a dose-dependent portal vasoconstriction which was antagonized both by haloperidol and by phentolamine. Since both of these antagonists attenuated the portal vasoconstrictor effects of intraportal phenylephrine, it is probable that the portal vasoconstriction effect of dopamine is due to alpha-adrenoceptor stimulation.
典型反应是起初的血管收缩,随后是更持久的血管舒张。这种血管舒张不受普萘洛尔影响,但被氟哌啶醇拮抗。起初的肝动脉血管收缩被氟哌啶醇和酚妥拉明均抑制。实验表明,起初的血管收缩是由于α-肾上腺素能受体刺激,而继发性血管舒张是多巴胺受体刺激的结果。在单独的实验中,将多巴胺注入犬的肝门静脉。观察到的唯一反应是剂量依赖性的门静脉血管收缩,它被氟哌啶醇和酚妥拉明均拮抗。由于这两种拮抗剂都减弱了门静脉内去氧肾上腺素的门静脉血管收缩作用,所以多巴胺的门静脉血管收缩作用很可能是由于α-肾上腺素能受体刺激。