Korner P I, Oliver J R, Reynoldson J A, Head G A, Carson V J, Walker M M
Eur J Pharmacol. 1978 Dec 15;53(1):83-93. doi: 10.1016/0014-2999(78)90270-4.
Acute effects of 6-hydroxydopamine (6-OHDA, 400--900 microgram kg-1 intracisternally, i.c.i.) consisted of bradycardia and hypertension, maximal 2--3 h after injection and preceded after some doses by a phase of hypotension. This pattern was obtained in completely conscious rabbits and after propanidid and sodium pentobarbitone anesthesia. After 600 microgram kg-1 i.c.i. 6-OHDA the peak rise in blood pressure (25 +/- 3.8 mm Hg) was due to a rise in peripheral resistance involving particularly renal and intestinal beds. Suprapontine mechanisms contributed to both hypertension and bradycardia. Giving pontine rabbits 6-OHDA elicited a short-latency fall in blood pressure, resembling the hypotensive phase in intact animals. Chronic effects 7 days after 600 microgram kg-1 included a rapid loss of 10% of body weight associated with reduction in food and water intake. To avoid secondary circulatory effects the rabbits were artificially fed, halving the weight loss. At 7 days blood pressure had fallen by 7.4 +/- 2.3 mm Hg probably owing to this residual weight loss. From experiments involving administration of phenotolamine and clonidine in intact rabbits and the responses of pontine animals it is likely that both descending and ascending catecholaminergic pathways have inhibitory effects on blood pressure, though some of the pathways may also be excitatory. Absence of specific chronic circulatory changes may be due to compensation through parallel pathways involving other transmitters.
6-羟基多巴胺(6-OHDA,脑池内注射400 - 900微克/千克)的急性效应包括心动过缓和高血压,注射后2 - 3小时达到峰值,某些剂量后会先出现一个低血压阶段。这种模式在完全清醒的兔子以及丙泮尼地和戊巴比妥钠麻醉后均能观察到。脑池内注射600微克/千克6-OHDA后,血压峰值升高(25±3.8毫米汞柱)是由于外周阻力增加,尤其是肾和肠血管床阻力增加所致。脑桥上机制对高血压和心动过缓均有影响。给脑桥动物注射6-OHDA会引发血压的短潜伏期下降,类似于完整动物的低血压阶段。600微克/千克剂量7天后的慢性效应包括体重迅速减轻10%,同时伴有食物和水摄入量减少。为避免继发循环效应,对兔子进行人工喂养,体重减轻减半。7天时血压下降了7.4±2.3毫米汞柱,可能是由于这种残留的体重减轻。从对完整兔子给予酚妥拉明和可乐定以及脑桥动物反应的实验来看,下行和上行的儿茶酚胺能通路可能对血压都有抑制作用,尽管其中一些通路也可能具有兴奋作用。缺乏特定的慢性循环变化可能是由于涉及其他递质的平行通路进行了代偿。