Montastruc J L, Rascol A, Montastruc P
Arch Mal Coeur Vaiss. 1981 Jun;74 Spec No:91-8.
The effects of bromocriptine administered by peripheral or central routes were studied in neurogenic hypertensive dogs. The acute hypertension was elicited by deafferentation (sino-aortic denervation). Intravenous (0,15 to 0,30 mg/kg) bromocriptine induced an important decrease in blood pressure of the debuffered dog (Fig. I). Bromocriptine reduced the arrhythmia induced by deafferentiation, but not the tachycardia of the debuffered dog (Table I). Bromocriptine was active by intracisternal route, at a dose (0,15 mg/kg) effective by intravenous route (Fig. 2). This antihypertensive effect of bromocriptine was also observed in debuffered dogs with binding of both vertebral and carotid arteries (i.e. when an effect of the drug on central structures was ruled out) (Fig. 3), and was suppressed by pretreatment with haloperidol, a dopaminergic antagonist (Fig. 4). These results imply that the mechanism underlying the hypotensive effect of bromocriptine is dopamine receptor stimulation; we consider that an effect on central nervous structures does not play a significant role in the hypotensive effect of this drug following acute intravenous administration in the dog.
研究了在外周或中枢途径给药的溴隐亭对神经源性高血压犬的影响。急性高血压通过去传入神经(窦主动脉去神经支配)诱发。静脉注射(0.15至0.30毫克/千克)溴隐亭可使去传入神经犬的血压显著降低(图1)。溴隐亭减少了去传入神经诱发的心律失常,但对去传入神经犬的心动过速没有影响(表1)。溴隐亭经脑池内途径给药时也有活性,其剂量(0.15毫克/千克)与静脉途径有效剂量相同(图2)。在双侧椎动脉和颈动脉结扎的去传入神经犬中(即排除药物对中枢结构的作用时)也观察到了溴隐亭的这种降压作用(图3),并且该作用被多巴胺能拮抗剂氟哌啶醇预处理所抑制(图4)。这些结果表明,溴隐亭降压作用的潜在机制是多巴胺受体刺激;我们认为,在犬急性静脉给药后,对中枢神经结构的作用在该药物的降压作用中不起重要作用。