Abstract

The pressor response to neostigmine after blockade of the ganglia by the administration of hexamethonium has been studied in dogs anesthetized with 30 mg/kg of sodium pentobarbital. The results have shown that after ganglionic blockade neostigmine will raise the blood pressure to levels approximating the pre-blockade level and restore the carotid occlusion response to approximately control values. The pressor response seen under these conditions is significantly greater than that obtained in dogs without ganglionic blockade and is blocked by the administration of atropine. This response was studied under a variety of different initial conditions to determine the possible site of action. It was found that the pressor response is not affected by prior adrenalectomy, the administration of small doses of phentolamine, Dibenamine or piperoxan, or the administration of blocking doses of β-TM-10 either alone or after adrenalectomy. The response is blocked by small doses of atropine and phenoxybenzamine. If the neostigmine is administered prior to the hexamethonium it does not block the hexamethonium-induced fall in blood pressure. This same pressor response may be obtained if other ganglionic blocking drugs are substituted for hexamethonium and if physostigmine is substituted for neostigmine. The possible mechanisms of this pressor response were discussed but no conclusion was reached as to the exact mechanism of action.