Is endotracheal adrenaline deleterious because of the beta adrenergic effect?

IV adrenaline increases coronary and cerebral perfusion pressures during ca rdiopulmonary resuscitation. We recently showed that endotracheal adrenalin e can decrease blood pressure (BP), a detrimental effect presumably mediate d by the beta2-adrenergic receptor unopposed by alpha -adrenergic vasoconst riction. This prospective, randomized, laboratory comparison of endotrachea l adrenaline (0.05 mg/kg diluted with normal saline to 10 mt total volume) with or without nonselective beta -blocker (propranolol) pretreatment was c onducted in an attempt to clarify the mechanism of this BP decrease. Five m ongrel dogs were given 0.05 mg/kg endotracheal adrenaline (diluted) or 0.05 mg/kg endotracheal adrenaline followed by an TV propranolol (0.1 mg/kg) pr etreatment. Each dog served as its own control (10 mt of normal saline admi nistered endotracheally) and received each regimen at least one week apart. Endotracheal adrenaline given after the propranolol pretreatment produced an increase in systolic, diastolic, and mean arterial BPs, from 165/110 mm Hg (mean 128 mm Hg) to 177.5/125 mm Hg (mean 142.5 mm Hg), respectively, as opposed to the hypotensive effect of isolated endotracheal adrenaline (P < 0.03). Thus, endotracheal adrenaline was associated with predominantly bet a -adrenergic-mediated effects, causing hypotension via peripheral vasodila tation unopposed by alpha -adrenergic vasoconstriction. The search for the optimal dose of endotracheal adrenaline should be aimed at achieving the hi gher alpha -adrenergic vasoconstrictive threshold.