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KMID : 0360419750110020019
Korean Journal of Pharmacology
1975 Volume.11 No. 2 p.19 ~ p.27
Experimental Studies on the Cardiovascular Effects of Haloperidol in Cat and Rabbit

Abstract
Haloperidol, a butyrophenone, was synthetized by Janssen and introduced for the treatment of psychosis. Although structurally different from the phenothiazines, the butyrophenones share many of their pharmacological properties, such as inhibition of conditioned avoidance response, blocking effect of amphetamine reaction, producing catalepsy, antishock effect and protection against the lethal effects of catecholamines.
Chlorpromazine can lower the arterial blood pressure through its adrenergic blocking activity, its direct effect in relaxing vascular smooth muscle, its direct effect in depressing the myocardium and its action in a complex manner on the central nervous system. In the case of haloperidol, however, was not clarified the mechanism of lowering the blood pressure.
The present paper describes the effects of haloperidol on cardiovascular system to investigate the mechanisms of its actions on the arterial blood pressure. The results are followings;
1. In anesthetized cats, intravenous administration of haloperidol and chlorpromazine in the dose of 0.1mg/kg produced a slight decrease in the blood pressure, which followed by complete recovery within 30~60 minutes. In the dose of 3mg/kg, however, both produced an abrupt and marked decrease of the blood pressure, which followed by delayed recovery.
2. Haloperidol in the dose ranges of 0.1mg to 3.0mg/kg tended to produce the heart rate slowing in the cats, while chlorpromazine has no effect on the rate.
3. following administration of haloperidol or chlorpiomazine, epinephrine reversal in the arterial blood pressure was observed In the cat, however the responses of norepinephrine and acetylchoine were little affected.
4. In the isolated rabbit atrium the contractility was depressed by haloperidol in the doses over 0.5mg per 100ml, but the rate was not affected. In contrast, the epinephrine-induced contractility was not depressed after heloperidol treatment. However, the increased rate of atrium by epinephrine was partially blocked after haloperidol.
5. In the isolated rabbit aortic strip, epinephrine-induced contraction was blocked by haloperidol.
With the above results, it may be concluded that the hypotensive effect of haloperidol was largely due to ¥á-adrenergic blocking properties and the direct effect in depressing the myocardium as well as its action on central nervous system.
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