Fagher B, Monti M, Thulin T
Department of Internal Medicine, University Hospital, Lund, Sweden.
Acta Med Scand. 1988;223(2):139-45.
Muscle thermogenesis was measured by direct microcalorimetry in hypertensive patients randomly treated with either metoprolol or placebo. Samples from rectus abdominis were taken after muscle relaxation during surgery, which was accompanied by a significant increase in arterial plasma noradrenaline. Thermogenesis was significantly lower in the metoprolol group compared with both the hypertensives given (p less than 0.05), and a normotensive group without treatment (p less than 0.005). Metoprolol also provoked a significant fall in body temperature in comparison with the two other groups (p less than 0.01). In the hypertensives given placebo, heat production was inversely related to plasma adrenaline (r = -0.89), indicating a role of the sympatho-adrenal system in muscle thermogenesis. No such correlation appeared during metoprolol treatment. In the present acute stress situation it is suggested that muscle thermogenesis was decreased indirectly by metoprolol via blockade of beta 1-receptors in adipose tissue, causing a relative inhibition of lipolysis with diminished substrate supply to the muscles.
通过直接微量热法对随机接受美托洛尔或安慰剂治疗的高血压患者的肌肉产热进行了测量。在手术期间肌肉松弛后采集腹直肌样本，此时动脉血浆去甲肾上腺素显著增加。与接受治疗的高血压患者（p<0.05）和未经治疗的正常血压组（p<0.005）相比，美托洛尔组的产热显著降低。与其他两组相比，美托洛尔还导致体温显著下降（p<0.01）。在接受安慰剂的高血压患者中，产热与血浆肾上腺素呈负相关（r = -0.89），表明交感-肾上腺系统在肌肉产热中起作用。在美托洛尔治疗期间未出现这种相关性。在当前的急性应激情况下，提示美托洛尔通过阻断脂肪组织中的β1受体间接降低肌肉产热，导致脂肪分解相对抑制，减少了向肌肉的底物供应。
