Intensification of the base deficit induced by vagotomy after atropine treatment in dogs.
The effects of atropine treatment on the heart rate, the arterial blood pressure, the respiratory rate, the acid-base profile and the oxygenation of arterial blood were investigated in chloralose anaesthetized dogs. As the I.V. atropine sulphate (1mg/kg) in saline (9% w/v) did not induce base deficit or alter the acid-base profile, the section of vagal parasympathetic (motor) fibres in normal (untreated) ones could not be held responsible for the observed base deficit after their vagotomy. Such observed base deficit was most likely engendered reflexively due to the section of vagal sensory fibres; as only general activation, not the withdrawal (section) of vagal sympathetic fibres might induce such an effect. Moreover, the bilateral vagotomy in these atropinized dogs induced a larger base deficit, which mostly contributed to the increase of H+ion concentration therein. This comparative enhancement of base deficit suggests that the opening of the negative feed back loop of the (aortic chemoreceptor) sensory fibres points to the blocking effect of atropine on the cholinergic link in the central (medulla) chemosensitive mechanism. The base excess observed after vagotomy in propranolol treated animals suggested that the base deficit vagal sensory fibres was mediated through reflexive activation of sympatho-adrenal axis.
D000136:Acid-Base Equilibrium / Q000187:drug effects*; D000818:Animals; D001285:Atropine / Q000494:pharmacology*; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000187:drug effects; D004285:Dogs; D006339:Heart Rate / Q000187:drug effects; D012119:Respiration / Q000187:drug effects; D014628:Vagotomy
D001285:Atropine