Late Breaking Abstract - Blockade of ß2-adrenoceptor augments anaphylaxis-induced increase in pulmonary vascular permeability in anesthetized mice

Abstract

Patients treated with propranolol, a nonselective β-adrenoceptor antagonist, develop severe anaphylaxis, but the mechanism remains unknown. We determined effects of β 1 - and β 2 -adrenoceptor antagonists on the anaphylaxis-induced increase in pulmonary vascular permeability in anesthetized ovalbumin-sensitized C57BL mice. Mean arterial blood pressure (MBP) was measured and Evans blue dye extravasation and hematocrit (Hct) were assessed at 20 min after antigen. The following 6 pretreatment groups (n=7/group) were studied: sensitized control (non-pretreatment), propranolol, the selective β 2 -adrenoceptor antagonist ICI 118,551, the selective β 1 -adrenoceptor antagonist atenolol, adrenalectomy, and non-sensitized. The antigen injection decreased MBP, and increased Hct and pulmonaary vascular permeability. In the propranolol, ICI 118,551 and adrenalectomy groups, the survival rate and Hct were smaller and greater, respectively, than that in the sensitized control group. Moreover, ICI 118,551, propranolol and adrenalectomy, but not atenolol, augmented the increase in pulmonary vascular permeability (Fig, 1). Plasma epinephrine levels increased significantly in the sensitize control mice. In conclusion, blockade of β 2 -adrenoceptor augments anaphylaxis-induced increase in pulmonary vascular permeability due to inhibition of beneficial effects of epinephrine released from adrenal glands in anesthetized mice.