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There are some observations which suggest the possibility of existence of cholinergic mediation in central integration of vomiting. Pilocarpine, a parasympathomimetic agent produces vomiting on intraventricular administration (1). Almost all the antiemetic agents possess antiacetylcholine activity to a varying degree. Moreover, central integration of vomiting occurs at the medullary level and it has been demonstrated that acetylcholine plays a mediator role in some of the medullary centers. We have shown that acetylcholine plays an excitatory transmitter role in the medullary vasomotor center (2). Varma (3) has provided evidence for cholinergic mediation in vagal nucleus. It was, therefore, thought worthwhile to investigate the role of acetylcholine in vomiting induced by various emetic agents using hemicholinium as a pharmacological tool. Methods and material: The present study was carried out in dogs of either sex weighing 7-12 kg. A metalic cannula was chronically implanted into one of the lateral cerebral ventricles by the method of Bhargava and Tangri (4). The reliability of the cannulation was tested by the emetic response to 1.0 pg of apomorphine given intracereventricularly (ICV) two days after implantation of the cannula. Only those dogs which gave a positive emetic response within 5 minutes of injection were included in the study. The animals were fed 30 minutes before eliciting an emetic response except in the case of copper sulfate which was given empty stomach. Hemicholinium (HC3) was injected ICV two hours before administering the emetic agents. The 100% effective emetic doses of apomorphine (5), sodium salicylate (6), ouabain (7) pilocarpine (1) protoveratrine (8) and copper sulfate (9) were used for eliciting the response.

EVIDENCE FOR ABSENCE OF CHOLINERGIC MEDIATION IN CENTRAL INTEGRATION OF VOMITING