Inhibition of cholesterol-induced increases in arterial wall permeability by propranolol

Increased arterial permeability to [125I]albumin is one of the earliest abnormalities found in the cholesterol-fed rabbit model for atherosclerosis and precedes morphologic changes in the arterial wall. Since propranolol is reported to retard atherogenesis in this model, the current study was undertaken to study the effect of propranolol on arterial permeability to albumin in cholesterol-fed rabbits. Carotid permeability to [125I]albumin was measured after 1 week of (a) a control diet containing only trace cholesterol (N = 9), (b) a 1.5% cholesterol diet (N = 11), or (c) a 1.5% cholesterol diet plus intraperitoneal propranolol 5 mg/kg/day (N = 19). The carotid artery was cannulated proximally and distally and peristaltically perfused with oxygenated Modified Eagle's Medium to which [125I]albumin had been added. The permeability of the carotid artery to albumin was estimated by measuring 125I activity in peripheral venous samples obtained after 0, 15, 30, 60, 120, 180, and 240 min of carotid perfusion. 125I-radioactivity of the perfused carotid artery was also counted at the end of the experiment to measure 125I retained in the arterial wall. The transfer of [125I]albumin across the arterial wall to the venous circulation was greater in the untreated cholesterol-fed group than in controls (P less than 0.05), but cholesterol-fed animals treated with propranolol did not differ significantly from controls. 125I-albumin in the arterial wall after 240 min of perfusion was decreased in both untreated cholesterol-fed animals (1444 dpm/cm +/- 350) and in propranolol-treated animals (1629 +/- 309) when these were compared to controls (3909 +/- 693, P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)