1 Binding of propranolol in vitro was determined in sera from 38 non-fasting patients 4-6 days after an acute myocardial infarction. The binding of propranolol was significantly lower in 12 patients receiving a subcutaneous heparin injection than in 26 patients receiving warfarin. 2 The binding of propranolol in sera from 9 geriatric patients without any acute diseases and 10 young, healthy subjects was similar to that of patients with acute myocardial infarction receiving heparin. 3 Mean serum concentration of α1-acid glycoprotein was similar in the four different groups of individuals. 4 For all subjects, the binding of propranolol was positively correlated to serum concentrations of α1-acid glycoprotein. 5 In the patients with myocardial infarction the binding was negatively correlated to serum concentrations of non-esterified fatty acids. Mean serum concentrations of non-esterified fatty acids was significantly higher in the patients receiving heparin than those receiving warfarin. 6 Addition of heparin and palmitic acid to serum in vitro did not affect the binding of propranolol. 7 The effect of heparin on binding variations was observed more closely in three non-fasting patients with myocardial infarction. Serum binding of propranolol and concentrations of chylomicrons and pre-β-lipoproteins were significantly reduced after a subcutaneous heparin injection of 5,000 iu, while serum concentrations of non-esterified fatty acids increased threefold. Concentrations of α1-acid glycoprotein and albumin were unchanged. Changes in binding of propranolol was closely correlated to concomitant changes in the triglyceride-rich lipoproteins. 8 These observations indicate that propranolol is bound to both triglyceride-rich lipoproteins and α1-acid glycoprotein in serum. Even smaller doses of heparin activate lipoprotein lipase and decrease binding of propranolol to lipoproteins in non-fasting subjects. |