title: Mechanism of chloramphenicol-induced modulation of mouse ileal motility.
abstract: The effect of chloramphenicol (CAP) on the intestinal motility of mice was studied. Acute and chronic CAP treatment significantly increased the food transit time. CAP produced concentration-dependent inhibition of motility of the isolated ileum of mice. Prazosin, propranolol, atropine, ouabain and chlorpromazine all failed to modulate or counteract the CAP-induced inhibition of ileal motility. However, naloxone and hexamethonium slightly modified the inhibitory response of CAP. The inhibitory response of CAP was markedly counteracted by cystine, a guanylate cyclase inhibitor. CAP increased the activity of Ca(++)-ATPase in the ileum in all experiments. Our results suggest that the CAP-induced inhibition of the intestinal motility is not mediated through adrenergic, cholinergic and cAMP or through inhibition of the electrogenic pump. Compared to thiamphenicol (TAP), CAP, with a p-NO2 group in its structure, exhibited more pronounced alteration of both intestinal motility and Ca(++)-ATPase activity. We, therefore, suggest that greater inhibition of ileal motility induced by CAP is possibly a p-NO2-cGMP-Ca(++)-ATPase-mediated mechanism.
mesh_terms: D018674:Adrenergic Antagonists / Q000494:pharmacology; D000818:Animals; D002701:Chloramphenicol / Q000494:pharmacology*; D005769:Gastrointestinal Motility / Q000187:drug effects*; D005772:Gastrointestinal Transit / Q000187:drug effects; D007082:Ileum / Q000187:drug effects* / Q000502:physiology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D013329:Structure-Activity Relationship; D013839:Thiamphenicol / Q000494:pharmacology
chemical_list: D018674:Adrenergic Antagonists; D002701:Chloramphenicol; D013839:Thiamphenicol