Tella S R, Schindler C W, Goldberg S R
Behavioral Pharmacology and Genetics Section, National Institute on Drug Abuse Addiction Research Center, Baltimore, MD 21224.
Pharmacol Res. 1993 Apr;27(3):233-9. doi: 10.1006/phrs.1993.1022.
Cocaine (0.3 mg/kg i.v.) produced prolonged pressor and tachycardiac responses in conscious squirrel monkeys. Peak pressor and tachycardiac responses following cocaine were 32.7 +/- 3.3 mm Hg and 78.8 +/- 7.4 beats/min, respectively. Pretreatment with 1 mg/kg chlorisondamine, a noncompetitive ganglionic blocker, attenuated the pressor (18.3 +/- 3.8 mm Hg) and tachycardiac (63.7 +/- 10 beats/min) effects of cocaine, while 5 mg/kg chlorisondamine completely prevented these effects of cocaine. This finding supports the conclusion that the cardiovascular effects of cocaine are centrally mediated.
可卡因（静脉注射0.3毫克/千克）在清醒的松鼠猴中产生了持久的升压和心动过速反应。可卡因给药后的升压和心动过速反应峰值分别为32.7±3.3毫米汞柱和78.8±7.4次/分钟。用1毫克/千克氯异吲哚铵（一种非竞争性神经节阻滞剂）预处理可减弱可卡因的升压作用（18.3±3.8毫米汞柱）和心动过速作用（63.7±10次/分钟），而5毫克/千克氯异吲哚铵则完全消除了可卡因的这些作用。这一发现支持了可卡因的心血管作用是由中枢介导的这一结论。
