Coltart D J, Shand D G
Br Med J. 1970 Sep 26;3(5725):731-4. doi: 10.1136/bmj.3.5725.731.
Plasma propranolol levels associated with reductions in endogenous and exogenous cardiac beta-stimulation were determined in normal people. The levels associated with a given degree of blockade of exercise-induced tachycardia were about three times greater after intravenous administration than after oral administration. This shows that an active metabolite of propranolol is formed only after the drug is taken by mouth. The greatest reduction in the tachycardia of strenuous exercise was associated with plasma levels of 40 ng./ml. with oral administration and 100 ng./ml. with intravenously administered propranolol.The effect on isoprenaline-induced tachycardia following intravenously administered propranolol showed that the dose ratio for isoprenaline was about 30 with plasma levels of 100 ng./ml. and 10 with levels of 10-20 ng./ml. These plasma levels give 100% and 20-30% blockade of exercise-induced tachycardia. These findings suggest that some of the therapeutic effects of propranolol may be unrelated to beta-adrenergic blockade.
在正常人中测定了与内源性和外源性心脏β刺激减少相关的血浆普萘洛尔水平。与一定程度的运动诱发心动过速阻滞相关的水平，静脉给药后比口服给药后大约高三倍。这表明普萘洛尔的活性代谢产物仅在药物口服后形成。剧烈运动心动过速的最大降低与口服给药时血浆水平40 ng/ml和静脉注射普萘洛尔时血浆水平100 ng/ml相关。静脉注射普萘洛尔后对异丙肾上腺素诱发心动过速的影响表明，当血浆水平为100 ng/ml时，异丙肾上腺素的剂量比约为30，当血浆水平为10 - 20 ng/ml时剂量比为10。这些血浆水平分别使运动诱发心动过速得到100%和20 - 30%的阻滞。这些发现提示普萘洛尔的某些治疗作用可能与β肾上腺素能阻滞无关。
