Pun K K, Yeung C K, Chak W, Ho P W, Chan M K, Lin H J, Yeung R T
Clin Nephrol. 1986 Nov;26(5):222-6.
Hypoglycemia is frequently reported in hemodialysis patients on propranolol. The effects of beta-blockers on the glucose, alanine and free fatty acid responses to glucagon challenge (2 mg) in fourteen hemodialysis patients were studied. Patients on propranolol had impaired glycemic response while those on metoprolol had decreased response only before dialysis. There was a significant negative correlation between propranolol level (log-transformed) and glycemic responses, suggesting that propranolol has direct effect on the latter. Hemodialysis patients had fasting alanine levels comparable to those of normal subjects. After glucagon challenge, the decrements in alanine level had no consistent relationship to the impaired glycemic response. Thus suppression of gluconeogenesis is unlikely to be the prime cause of propranolol-induced hypoglycemia. The basal free fatty acid levels were significantly lower among hemodialysis patients on propranolol. This limited availability of free fatty acid as well as the inhibitory effect on hepatic glucagon-stimulated glucose output may contribute to the predisposition to hypoglycemia in dialysis patients given propranolol. The results suggest that metoprolol has less interference on energy substrate supply in hemodialysis patients under fasting conditions.
血液透析患者服用普萘洛尔时低血糖情况屡有报道。研究了β受体阻滞剂对14例血液透析患者在胰高血糖素激发试验(2毫克)中葡萄糖、丙氨酸和游离脂肪酸反应的影响。服用普萘洛尔的患者血糖反应受损,而服用美托洛尔的患者仅在透析前反应降低。普萘洛尔水平(对数转换)与血糖反应之间存在显著负相关,表明普萘洛尔对后者有直接影响。血液透析患者的空腹丙氨酸水平与正常受试者相当。胰高血糖素激发试验后,丙氨酸水平的下降与受损的血糖反应没有一致的关系。因此,糖异生的抑制不太可能是普萘洛尔诱发低血糖的主要原因。服用普萘洛尔的血液透析患者基础游离脂肪酸水平显著较低。游离脂肪酸的这种有限可用性以及对肝脏胰高血糖素刺激的葡萄糖输出的抑制作用可能导致服用普萘洛尔的透析患者易发生低血糖。结果表明,在禁食条件下,美托洛尔对血液透析患者能量底物供应的干扰较小。