The effect of reduced perfusion pressure and regional sympathetic vasoconstrictor activation on the rate of absorption of 85Kr from the small intestine of the cat.
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Biomedical subjects
Publications and source records attributed to J Svanvik.
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Inflammatory fluid secretion by the gallbladder mucosa in experimental cholecystitis is induced by activation of cyclooxygenase, which leads to an increase in prostaglandin formation. Cyclooxygenase exists as a constitutive (cyclooxygenase-l) and an inducible (cyclooxygenase-2) isoform. The aim of this study was to demonstrate the role of cyclooxygenase-2 in inflammatory fluid secretion of the feline gallbladder. Experiments were performed 10 weeks after a surgical procedure in which chronic cholecystitis was induced in cats by ligation of the cystic duct and implantation of a gallstone in the gallbladder. Gallbladder fluid transport was continuously monitored via a perfusion system. In inflammed gallbladders the continuous fluid secretion was reversed to absorption by intravenous injection of the selective cyclooxygenase-2 blocker, NS 398 (P <0.001). Increased levels of the inducible cyclooxygenase-2 were shown by immunoblotting in inflamed gallbladders. Selective pharmacologic blockage of cyclooxygenase-2 reduced the prostaglandin E2 release to the inflamed gallbladder lumen (P <0.01). These data suggest that cyclooxygenase-2 is involved in the inflammatory response during chronic cholecystitis. Selective cyclooxygenase-2 blockers may offer an alternative to traditional nonsterodial anti-inflammatory drugs with fewer side effects in patients with cholecystitis who are awaiting operation.
A case of hypercholeresis following release of protracted extrahepatic obstruction causing dehydration and metabolic acidosis is described. Possible background mechanisms for post-cholestasis hypercholeresis are briefly discussed.
A case of intussusception at four different locations in the small intestine is reported. Operative reduction of the interponates were performed with an uneventful postoperative course. The treatment of intussusception in adults is discussed and the literature is reviewed.