Pharmacological modulation of 86Rb efflux from aortic endothelial cells.

The ATP-induced efflux of 86Rb from prelabelled bovine aortic endothelial cells was inhibited by quinine (50 microM) but not by a tetraethylammonium (5 mM) or apamin (50 nM). Neither sulfonylureas nor pinacidil had a significant effect on the rate of 86Rb efflux from the endothelial cells. These data are consistent with the presence of intermediate conductance Ca2(+)-activated K+ channels in endothelial cells. ATP-dependent K+ channels, sensitive to sulfonylureas and pinacidil, could not be detected.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe

Effects of changes in extra- and intracellular K+ on the endothelial production of prostacyclin.

1. Changes in the KCl concentration of the incubation medium, from 0 to 80 mM, had no effect on the basal or ATP-stimulated release of prostacyclin (PGI2) from bovine aortic endothelial cells. 2. The monovalent cation ionophores, valinomycin and nigericin (5 microM), enhanced the release of PGI2 from endothelial cells stimulated by ATP or bradykinin. 3. The action of nigericin, unlike that of valinomycin, was time-dependent, abolished in a high-KCl medium and associated with an increased efflux of 86Rb and a time-dependent depletion of intracellular K+. 4. Ouabain (1-100 microM) also enhanced the release of PGI2 in response to ATP and induced a significant depletion of intracellular K+ in bovine aortic endothelial cells. 5. In conclusion, modifications of the endothelial cell membrane potential, resulting from changes in the extracellular K+ concentration, do not modulate the basal or ATP-stimulated production of PGI2. An acute depletion of intracellular K+ by nigericin or ouabain enhances the production of PGI2 in aortic endothelial cells stimulated by ATP or bradykinin.Journal ArticleResearch Support, Non-U.S. Gov'tFLWINinfo:eu-repo/semantics/publishe

Enhanced release of prostacyclin from quin 2-loaded endothelial cells.

The acetoxymethyl ester (AM) of quin-2 (quin-2/AM) enhanced the release of prostacyclin (PGI2) from bovine aortic endothelial cells stimulated by ATP, bradykinin or ionophore A23187. It also increased the mobilization of free arachidonic acid in response to ATP. Ca2+-clamping with a combination of EGTA and quin-2/AM abolished the response to ATP. The effect of quin-2/AM was mimicked by a structural analog, the acetoxymethyl ester of 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA/AM), but not by the heavy metal chelator, tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) and only slightly by fura-2/AM. The mechanism of this pharmacological action of quin-2/AM and its potential for the design of PGI2-stimulating drugs remain to be explored.In VitroJournal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe

Nation-wide prospective surveillance of Clostridium difficile infections in hospitals in Belgium, July 2007-June 2008.

We report here baseline data from the first year of compulsory surveillance of Clostridium difficile infections (CDI) in hospitals in Belgium. Between 1 July 2007 and 30 June 2008, 2,704 CDI were reported: 12% were recurrent and 66% were hospital-associated (half of which occurred 15 days or more after admission). CDI was considered the cause of death (direct or indirect) for 10% of the episodes. The median incidence of CDI was 1.5 per 1,000 admissions and 1.9 per 10,000 hospital-days for all cases, and 0.9 per 1,000 admissions, and 1.1 per 10,000 hospital-days for hospital-associated cases. Further investigation of risk stratification by average length of stay in the reporting hospitals is warranted as a way to improve the comparability of indicators across hospitals and surveillance systems. In spite of methodological issues, the surveillance of CDI in Belgian hospitals has been able to produce robust baseline data that should allow monitoring of trends at hospital and national level, and provide a basis for international comparisons. Remaining challenges are to define and monitor targets for the control of CDI, and to improve the individual feed-back of data at hospital level

Acquired pancreatic arteriovenous malformation

Pancreatic arteriovenous malformation is a rare vascular anomaly which may cause abdominal pain, acute pancreatitis, gastrointestinal bleeding and portal hypertension. Pancreatic arteriovenous malformation is mostly congenital; however secondary pancreatic arteriovenous malformation due to pancreatitis has been suggested by some authors. We encountered a case which can confirm this presumption. Several imaging modalities are useful for the diagnosis of pancreatic arteriovenous malformation, especially dynamic contrast-enhanced studies. Angiography is the most important diagnostic tool because of the dynamic features of this vascular lesion. Treatment is advised and consists of surgical resection and/or transarterial embolization