Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008325 (cholecystitis)
 3,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Continuing evaluation of the pathophysiology of gallbladder disease has demonstrated significant relationships between gallbladder mucosal fluid transport, gallbladder inflammation, and prostanoid formation. Inflamed gallbladder mucosa secretes, rather than absorbs, fluid, a process associated with prostaglandin formation. Bradykinin has been previously implicated in the pathogenesis of cholecystitis and, in the intestine, bradykinin stimulates mucosal fluid secretion by a prostaglandin-mediated mechanism. Bradykinin was infused into the gallbladder lumen and administered intraarterially into the hepatic artery of perfused cat gallbladders. Both methods of bradykinin administration reversed the mucosal absorption present during control experiments as measured by concentration changes in a nonabsorbable marker. Perfusate and gallbladder tissue prostaglandin E concentrations were significantly increased by bradykinin when compared to control values. Concentrations of 6-keto PGF1 alpha in perfusate solutions and in gallbladder tissue were significantly increased, suggesting bradykinin increased prostacyclin formation. Bradykinin administration significantly increased inflammation, as evaluated by a histologic scoring system. Indomethacin was administered intravenously along with luminal perfusion of the gallbladder with bradykinin. Indomethacin significantly decreased gallbladder fluid secretion and prostanoid formation, but not histologic inflammation, when compared to values produced by bradykinin alone. An increase in systemic vascular and bile kinin concentrations produces gallbladder mucosal water secretion, a process which may be mediated by prostanoids. Histologic inflammation produced by bradykinin was not prevented by indomethacin.
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PMID:Effect of bradykinin on feline gallbladder water transport and prostanoid formation. 258 88

Neurogenic inflammation implies stimulation of nerves with resultant inflammation in tissue surrounding the nerve terminals. We hypothesized that neurogenic inflammation has a role in cholecystitis. Capsaicin (stimulant of afferent, nociceptive neurons), 6-hydroxydopamine (stimulates release of peptides from sympathetic nerve terminals), bradykinin, lipopolysaccharide, and saline were instilled into guinea pig gallbladders for 24 hr (N = 5 in each group). In parallel, test agents were instilled with 1% Iidocaine. Water transport across gallbladder mucosa, myeloperoxidase and interluekin-1 release from gallbladder tissue, and prostaglandin E2 in luminal fluid were measured. Capsaicin caused water secretion and significant release of myeloperoxidase, interleukin-1, and prostaglandin-E2, effects that were blocked by Iidocaine. 6-Hydroxydopamine did not affect water transport or prostaglandin E2, but did cause myeloperoxidase and interleukin-1 release. Bradykinin- and lipopolysaccharide-induced inflammation were partially inhibited by lidocaine. Taken together, these results suggest that neurogenic inflammation has a role in the pathophysiology of cholecystitis.
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PMID:Neurogenic inflammation in cholecystitis. 924 52