Selective beta 1-adrenoceptor blockade and muscle thermogenesis.

Acta medica Scandinavica Pub Date : 1988-01-01
B Fagher, M Monti, T Thulin
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Abstract

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.

选择性β 1-肾上腺素能受体阻断与肌肉产热。
在随机接受美托洛尔或安慰剂治疗的高血压患者中,用直接微量热法测量肌肉产热。手术中肌肉松弛后取腹直肌标本,伴动脉血浆去甲肾上腺素显著升高。美托洛尔组与高血压组和未治疗的正常血压组相比,生热性明显降低(p < 0.05)。与其他两组相比,美托洛尔组的体温也显著下降(p < 0.01)。在给予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的作用。在美托洛尔治疗期间没有出现这种相关性。在目前的急性应激情况下,这表明美托洛尔通过阻断脂肪组织中的β 1受体间接减少了肌肉产热,导致脂肪分解的相对抑制,减少了对肌肉的底物供应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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