Mueller H S, Ayres S M
J Clin Invest. 1980 Feb;65(2):338-46. doi: 10.1172/JCI109677.
Plasma 1-norepinephrine and epinephrine contents were strikingly elevated in 70 patients during evolution of myocardial infarction. Propranolol or placebo, 0.1 mg/kg i.v., was administered randomly an average of 10 h after infarction and continued orally for 3 d. Propranolol, but not placebo, acutely decreased 1-norepinephrine contents from 2.24 +/- 1.33 (mean +/- SD) to 1.31 +/- 0.74 microgram/liter, P less than 0.001, and epinephrine contents from 0.97 +/- 0.42 to 0.74 +/- 0.42 microgram/liter, P less than 0.02. Decreases in 1-norepinephrine contents were related to the initial plasma concentrations, r = 0.85, P less than 0.001. A similar, but less strong relationship was observed between the initial epinephrine contents and propranolol-induced changes, r = -0.51, P less than 0.01. Propranolol reduced plasma-free fatty acid contents from 1,121 +/- 315 to 943 +/- 274 mumol/liter, P less than 0.001. Decreases in plasma contents of free fatty acids were related to decreases in epinephrine, r = 0.66, P less than 0.001. Propranolol did not cause significant additional changes in plasma catecholamine contents during the subsequent 3 d. In the placebo group 1-norepinephrine contents had decreased 24 h after infarction from 1.92 +/- 0.99 to 1.37 +/- 0.93 microgram/liter, P less than 0.02. Plasma epinephrine contents did not change. Heart rate remained below the control values during the entire study period in the propranolol, but increased in the placebo group. The data indicate that sympathetic hyperactivity, indirectly reflected by plasma catecholamine contents, is acutely reduced by propranolol during evolution of myocardial infarction.
在70例心肌梗死患者病情演变过程中，血浆去甲肾上腺素和肾上腺素含量显著升高。梗死平均10小时后，随机静脉注射普萘洛尔或安慰剂，剂量为0.1mg/kg，并持续口服3天。普萘洛尔可使去甲肾上腺素含量从2.24±1.33（均值±标准差）微克/升急剧降至1.31±0.74微克/升，P<0.001；肾上腺素含量从0.97±0.42微克/升降至0.74±0.42微克/升，P<0.02。去甲肾上腺素含量的降低与初始血浆浓度相关，r=0.85，P<0.001。初始肾上腺素含量与普萘洛尔诱导的变化之间也观察到类似但较弱的关系，r=-0.51，P<0.01。普萘洛尔使血浆游离脂肪酸含量从1121±315微摩尔/升降至943±274微摩尔/升，P<0.001。血浆游离脂肪酸含量的降低与肾上腺素的降低相关，r=0.66，P<0.001。在随后3天内，普萘洛尔未引起血浆儿茶酚胺含量的显著额外变化。在安慰剂组，梗死24小时后去甲肾上腺素含量从1.92±0.99微克/升降至1.37±0.93微克/升，P<0.02。血浆肾上腺素含量未改变。在整个研究期间，普萘洛尔组心率一直低于对照值，而安慰剂组心率增加。数据表明，在心肌梗死演变过程中，普萘洛尔可急性降低由血浆儿茶酚胺含量间接反映的交感神经功能亢进。
