No abstract available.
Respiratory Tract Infections*

Severe intraoperative hypotension has been reported in patients on angiotensin-converting enzyme inhibitors and angiotensin II receptor subtype 1 antagonists. We describe a patient on lisinopril who developed refractory intraoperative hypotension associated with increased serum tryptase level suggesting mast cell activation (allergic reaction). However, allergology workup ruled out an allergic etiology as well as mastocytosis, and hypotension recalcitrant to treatment was attributed to uninterrupted lisinopril therapy. Elevated serum tryptase was attributed to our patient's chronic renal insufficiency.
Anaphylaxis ; Angiotensin-Converting Enzyme Inhibitors ; Humans ; Hypotension ; Lisinopril ; Mast Cells ; Mastocytosis ; Receptors, Angiotensin ; Renal Insufficiency, Chronic ; Tryptases

Endoscopic ultrasonography-guided gastroenterostomy using a lumen-apposing metal stent has emerged as a novel technique in the palliative treatment of malignant gastric outlet obstruction. Endoscopic ultrasonography-guided gastroenterostomy seems to have the potential to provide long-lasting patency in a minimally invasive manner. Low reintervention rates have been described. We report two cases with early lumen-apposing metal stent dysfunction, compromising patency. One case showed food impaction after three weeks, and hyperplastic tissue overgrowth with a buried distal flange six weeks after stent placement. The latter was successfully treated by argon plasma coagulation, stent removal, and deployment of a larger-diameter lumen-apposing metal stent. The second case showed a narrowed luminal diameter of the stent and jejunal pressure ulcerations after three weeks. The narrowing was successfully treated by balloon dilation. Eight weeks later, hyperplastic tissue overgrowth at the distal flange of the stent and a gastro-colonic fistula were diagnosed, followed by extensive reconstructive surgery.

Endoscopic ultrasonography-guided gastroenterostomy using a lumen-apposing metal stent has emerged as a novel technique in the palliative treatment of malignant gastric outlet obstruction. Endoscopic ultrasonography-guided gastroenterostomy seems to have the potential to provide long-lasting patency in a minimally invasive manner. Low reintervention rates have been described. We report two cases with early lumen-apposing metal stent dysfunction, compromising patency. One case showed food impaction after three weeks, and hyperplastic tissue overgrowth with a buried distal flange six weeks after stent placement. The latter was successfully treated by argon plasma coagulation, stent removal, and deployment of a larger-diameter lumen-apposing metal stent. The second case showed a narrowed luminal diameter of the stent and jejunal pressure ulcerations after three weeks. The narrowing was successfully treated by balloon dilation. Eight weeks later, hyperplastic tissue overgrowth at the distal flange of the stent and a gastro-colonic fistula were diagnosed, followed by extensive reconstructive surgery.

<b>BACKGROUNDb>Batroxobin (BX), a serine protease used in defibrinogenation and thrombolysis, also has an effect on c-fos gene and growth factor. This study attempted to determine the effects of BX on the proliferation of vascular smooth muscle cells (VSMCs) and calcium metabolism.

<b>METHODSb>VSMCs were treated with BX at concentrations of 0.1, 0.3, or 1.0 mmol/L and cell numbers were determined at 0, 24, 48, and 72 hours. Intracellular calcium concentration ([Ca2+]i) was measured using direct fluorescence methods.

<b>RESULTSb>BX was found to suppress proliferation of VSMCs in a dose-dependent fashion with inhibition rates of 18% and 31% by 48 and 72 hours, respectively. In addition, BX decreases basal [Ca2+]i significantly. The basal level in untreated cells was 162.7 +/- 33.8 nmol/L, and decreased to 131.5 +/- 27.7 nmol/L, 128.3 +/- 28.5 nmol/L, and 125.6 +/- 34.3 nmol/L with the three concentrations of BX, respectively. Noradrenaline (NE)-induced [Ca2+]i stimulation was also attenuated by BX (0.1 mmol/L BX, 20% +/- 8% inhibition; 0.3 mmol/L BX, 54% +/- 11% inhibition; 1.0 mmol/L BX, 62% +/- 15% inhibition). The ability of NE to stimulate [Ca2+]i was attenuated in cultures in Ca(2+)-free medium, as was the ability of BX to blunt NE-induced stimulation.

<b>CONCLUSIONb>These findings demonstrate that BX can effectively inhibit proliferation of VSMCs, probably by blocking the release and uptake of Ca2+, thus influencing [Ca2+]i.

Animals ; Batroxobin ; administration & dosage ; pharmacology ; Calcium ; metabolism ; Cell Division ; drug effects ; Cells, Cultured ; Dose-Response Relationship, Drug ; Muscle, Smooth, Vascular ; cytology ; metabolism ; Rabbits