β-Adrenoceptor activity and resting energy metabolism in weight losing cancer patients

被引:47
作者
Hyltander, A
Daneryd, P
Sandström, R
Körner, U
Lundholm, K [1 ]
机构
[1] Sahlgrens Univ Hosp, Surg Metab Res Lab, S-41345 Gothenburg, Sweden
[2] Sahlgrens Univ Hosp, Lundberg Lab Canc Res, Dept Surg, S-41345 Gothenburg, Sweden
基金
英国医学研究理事会;
关键词
cachexia; indirect calorimetry; beta-adrenoceptor;
D O I
10.1016/S0959-8049(99)00273-7
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
This study was aimed at comparing the blocking of beta-adrenoceptor activity to changes in the resting energy metabolism of 10 cancer patients with progressive weight loss due to solid malignant tumours. Resting energy expenditure (REE) as well as whole body carbohydrate and fat oxidation were investigated and related to plasma substrate levels (glucose, glycerol, free fatty acids (FFA)) before and after 5 days of oral administration of specific beta 1 receptor blocker (atenolol, 50 mg/day) and non-specific beta 1.beta 2- adrenoceptor (propranolol. 80 mg/day) blockade. The administration order of the drugs was random, and a 3-day washout period was used in all individuals between the provision of the first and the second drug in order to minimise the risk of carry-over effects. Resting measurements in the morning after an overnight fast were performed by indirect calorimetry. Atenolol treatment reduced REE by 77 +/- 14 kcal:day and propranolol by 48 +/- 13 kcal/day. respectively (P < 0.05 versus pretreatment values). Whole body oxygen uptake and carbon dioxide production were decreased similarly by both atenolol and propranolol treatment (P < 0.05). Carbohydrate oxidation was increased by atenolol and decreased by propranolol, whilst fat oxidation was decreased by atenolol and unchanged by propranolol. The decrease in REE, accounting for the decline in heart rate, was significantly mort pronounced following treatment with propranolol compared with atenolol (P < 0.05). Atenolol and propranolol had no effect on blood glucose, plasma glycerol and FFA. We conclude that wastage in cancer patients is in part explained by increased beta(1) and beta(2)-adrenoceptor activity, in part secondary to elevated cardiovascular activity as a result of anaemia, loss of cardiac contractile capacity and altered host metabolism. (C) 2000 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:330 / 334
页数:5
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