Buylaert W A
Naunyn Schmiedebergs Arch Pharmacol. 1977 Aug;299(1):101-3. doi: 10.1007/BF00508645.
On local injection into the innervated hindleg of the dog piribedil, like apomorphine, produced a vasodilatation blocked by haloperidol. S584, the catechol metabolite of piribedil, produced a vasodilatation which was not blocked by haloperidol. Neither propranolol nor atropine influenced the vasodilatation produced by piribedil or S584. Denervation of the hindleg abolished the responses to piribedil and S584. During the infusion of noradrenaline into the denervated hindleg, the responses to S584 reappeared but those to piribedil did not. It is concluded from these experiments that the vasodilatation produced by piribedil in the innervated hindleg of the dog, like that of apomorphine, is mediated by dopamine receptors and that the effect of piribedil cannot be explained by the formation of its catechol metabolite S584.
在对狗的受神经支配的后肢进行局部注射时，匹立哌唑与阿扑吗啡一样，会引起血管舒张，且这种血管舒张会被氟哌啶醇阻断。S584是匹立哌唑的儿茶酚代谢产物，它引起的血管舒张不受氟哌啶醇的阻断。普萘洛尔和阿托品均不影响匹立哌唑或S584所引起的血管舒张。后肢去神经支配消除了对匹立哌唑和S584的反应。在向去神经支配的后肢输注去甲肾上腺素期间，对S584的反应重新出现，但对匹立哌唑的反应未出现。从这些实验得出的结论是，匹立哌唑在狗的受神经支配的后肢中引起的血管舒张，与阿扑吗啡的情况一样，是由多巴胺受体介导的，并且匹立哌唑的作用不能用其儿茶酚代谢产物S584的形成来解释。
